Benefits of Chlorophyllin Detoxifies Liver Eliminates Body Odor Cleans Digestive Tract Can prevent Liver and other Cancers Used in Cancer Therapy Good for Anemia Eliminates Mold toxins from Body

Fact - Chlorophyll(ins)
can help prevent Cancer

Science has known for years that without chlorophyll, the 'green blood' of plant / photosynthesis, life as we know it could not exist. Until recently, most research involving plants has been geared towards 'better plants' for 'better meat'".  For years it was thought that the protein we needed could only come from meat. This website brings together the research that proves different, such is the case in evolution.

In the 1960s poultry farmers in the UK and trout farmers in the pacific northwest of the United States began losing their stock to an unknown illness. The culprit was identified as the fungus Aspergillus Flavus and a toxic metabolite it produces called Aflatoxin B1, one of the most potent human carcinogens.  The trout were subsequently discovered to be extremely sensitive to Aflatoxin B1 and an excellent model for environmental carcinogenesis research.

In the mid-80s, Dr. Roderick Dashwood, familiar with the anti-mutagenic abilities of chlorophylls in bacterial assays, began to study the possible benefits of chlorophyllins (a chlorophyll derivative commonly extracted from the alfalfa plant) given to trout exposed to Aflatoxin B1. The results of Dr. Dashwood and his colleagues were the first scientific confirmation of the chemo-protective effect of chlorophylls. Since then, research has continued using a multitude of cancer causing substances. The results are the same ...

 CHLOROPHYLLIN HELPS PREVENT CANCER! 

Unbelievably 'Chlorophyllin' is virtually unheard of. Nutrition councils recommend 5-10 servings of fruits and vegetables daily with particular emphasis on 'greens'. Unfortunately, to obtain the benefits found in one dose of Chlorophyllin you would have to consume massive amounts of fresh or frozen produce. In fact, it takes approximately 400 lbs of raw material (alfalfa) to make 1 lb of Chlorophyllin.

Now that the facts are in, we hope that the medical profession will soon be singing the praises of this natural, non-toxic wonder.   The information on this website will prove to be invaluable to you and your loved ones. It is our hope, and our quest, that every home in every country in every nation has access to this powerful protector, simple inexpensive bottles of Liquid Chlorophyll (Sodium Copper Chlorophyllin). If our voice is heard,  most every known disease will/can be prevented or cured.

Liquid Chlorophyllin, a remarkable product derived from Medicago Sativa Leaf, has proven to be one of the most powerful antioxidants AND studies have shown that it can prevent cancer.  Just 300 milligrams per day (3 tbsp) can reduce your risk of cancer dramatically.

Chlorophyllin knocks out dietary toxins (which account for 30-40% of all cancers) fighting in at least two arenas. First, Chlorophyllin forms irreversible complexes with some cancer causing substances that we ingest before they enter the bloodstream (think of Velcro) and they are safely eliminated from the body.  Secondly, as an antioxidant, Chlorophyllins neutralize free radicals within the body that could otherwise cause cell mutations that can lead to cancer.
 

Heme Molecule in Blood	Chlorophyll Molecule

Is ‘Chlorophyllin’ the same as chlorophyll? Not quite.  The chlorophyll molecule in its natural state contains a magnesium center and is not water-soluble.  Scientists are unsure just how much, if any, enters the bloodstream.  Chlorophyllin molecules on the other hand, are able to travel throughout the body as the magnesium center has been replaced with copper. Copper, like iron, is an oxygen transporter. In fact, the chlorophyllin molecule is almost identical to the heme molecule in our blood. 

Oxygenate yourself with Oxygenz Liquid Chlorophyllin!  It is so simple to incorporate our Oxygenz Liquid Chlorophyllins into your daily routine.  Like our Phytogenz Powder, it can be added to your favorite beverage and enjoyed any time of day.  Detoxify, improve circulation and regularity, eliminate body odor, help treat anemia, improve hemoglobin levels (especially during chemotherapy).

In vitro studies with chlorophyllin show it to be an inhibitor of the cytochrome P-450 liver enzymes (Tachino et al. 1994). All in vivo [whole animal] studies where cytochrome P-450 enzyme activity is reduced resulted in lower cancer rates and longer lifespan (Guengerich et al. 1991). In Stage 2 liver detoxification, enzymes called glutathione transferases cause glutathione to react with the carcinogens formed from cytochrome P-450 activity to produce harmless additional products, but this process is not very efficient (Finch et al. 1997). Chlorophyllin, however, makes this conversion more efficient by lowering cytochrome P-450 enzyme activity in the first place and by reacting with carcinogens to produce harmless complexes, just as the glutathione transferases do. Thus, chlorophyllin is not an inducer of glutathione transferases but mimics glutathione transferase activity.

Effect of cancer chemopreventive agents on microsome-mediated DNA adduction of the breast carcinogen dibenzo[a,l]pyrene.
Smith WA, Arif JM, Gupta RC.

Graduate Center for Toxicology, University of Kentucky Medical Center, Lexington 40536-0305, USA.

Due to the large and expanding number of potential cancer chemopreventive agents, there is an increasing need for short term tests to study the efficacy and mechanisms of these agents. In this study, we have employed a microsome-mediated test system to study the effect of several suspected chemopreventive agents on the DNA adduct formation capacity of the potent mammary carcinogen, dibenzo[a,l]pyrene (DBP). Bioactivation of DBP by Aroclor 1254-induced rat liver microsomes in the presence of calf thymus DNA (300 microg/ml) resulted in the formation of one major and six other prominent DNA adducts (324 adducts/10(7) nucleotides). These adducts were previously determined to be deoxyadenosine (dA) and deoxyanosine (dG)-derivatives of both anti- and syn-DBP-11,12-diol-13,14-epoxides (DBPDE). Intervention with ellagic acid, chlorophyllin, benzyl isocyanate (BIC), oltipraz or genistein (150 microM) strongly diminished DBP-DNA adduction by > or = 75%. Linoleic acid, curcumin and butylated hydroxytoluene (BHT) also significantly inhibited DBP DNA adduction (26-46%) while N-acetylcysteine (NAC) had no effect. Moreover, nonenzymatic studies with anti- and syn-DBPDE isomers revealed that chlorophyllin, ellagic acid, BIC and BHT may be inhibiting DBP-DNA adduction in an enzymatic-independent manner since these agents diminished DBPDE-DNA adduction by 30-75%. Genistein, oltipraz and curcumin did not diminish DBPDE-DNA adduction and therefore most likely require the presence of the microsomal subcellular fraction to inhibit DBP-DNA adduction.
 

Early detection and prevention of colorectal cancer (review).
Dashwood RH.

The Linus Pauling Institute, Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331-6512, USA.

Colorectal cancer is a leading cause of cancer-related deaths, and the two most important considerations for avoidance of this disease are early detection and prevention. If metastasis has occurred to distant sites, such as the liver and lung, the 5-year survival rate for colorectal cancer is below 10%, but this increases to greater than 90% when the cancer is found early. Early detection can be facilitated by use of the digital rectal exam, fecal occult blood test, sigmoidoscopy, and colonoscopy, but these methods might be supplemented in the future by other screening assays using intermediate biomarkers. One interesting biomarker, the aberrant crypt focus (ACF), has been observed in resected human colons, and is the earliest detectable morphological change in the colons of experimental animals treated with carcinogens such as the cooked meat heterocyclic amines. The ACF can also be used as an end-point to screen for potential inhibitors of colorectal cancer; using this approach, we identified conjugated linoleic acids, indole-3-carbinol, chlorophyllin, and tea polyphenols as promising inhibitors in the colon. These compounds can be added to a growing list of natural and synthetic agents that might be effective against colorectal cancer, including selenium, calcium, and nonsteroidal anti-inflammatory agents. However, results from human clinical trials with several of these compounds have highlighted the need for detailed mechanism data before recommendations can be made for wide-scale use in humans. In the meantime, the best approach to reducing the risk of colorectal cancer would be to increase the dietary intake of fruits, vegetables and cereals, while reducing the overall intake of fat, particularly from animal sources.
 

Inhibition of radiation-induced DNA damage in plasmid pBR322 by chlorophyllin and possible mechanism(s) of action>
Kumar SS, Chaubey RC, Devasagayam TP, Priyadarsini KI, Chauhan PS.

Cell Biology Division, Bhabha Atomic Research Centre, Mumbai 400 085, India.

Naturally occurring compounds capable of protecting DNA against ionizing radiation and chemical mutagens have considerable potential for prevention of mutation-based health impairment including cancer and other degenerative diseases. Chlorophyllin (CHL), a water-soluble derivative of chlorophyll, has been examined for its ability to protect DNA against radiation induced strand breaks using an in vitro plasmid DNA system. Gamma-radiation, up to a dose of 6 Gy (dose rate 1.25 Gy/min), induced a dose-dependent increase in single-strand breaks (ssbs) in plasmid pBR322 DNA. CHL per se did not induce, but inhibited radiation-induced ssbs in a concentration-dependent manner; 500 microM giving about 90% protection. The protection afforded by CHL was comparatively less than that of trolox, a water-soluble analogue of alpha-tocopherol. To elucidate the underlying mechanism(s), reaction of CHL with the radiation-derived hydroxyl radical (.OH) and deoxyribose peroxyl radical (ROO.) was studied by pulse radiolysis. CHL exhibited a rate constant of 6.1+/-0.4x109 M-1 s-1 with.OH and 5.0+/-1.3x107 M-1 s-1 with ROO. To our knowledge, this is the first report providing direct evidence of free radical-scavenging properties of CHL. The results showed that CHL, effectively protects plasmid DNA against ionizing radiation, in an in vitro system independent of DNA repair or other cellular defense mechanisms. The ability of CHL to scavenge. OH and ROO., may contribute to its protective effects against radiation induced DNA damage in the pBR322 system.

Chemoprevention studies of heterocyclic amine-induced colon carcinogenesis.
Xu M, Dashwood RH.

The Linus Pauling Institute, and Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis 97331-6512, USA.

The cooking of meat and fish produces heterocyclic amine mutagens, including 2-amino-1-methyl-6-phenylimidazo[4,5b]pyridine (PhIP) and 2-amino-3-methylimidazo[4,5-f]quinoline (IQ). Chronic administration of PhIP or IQ to the F344 rat induces tumors at several sites, including adenocarcinomas of the colon, and short-term treatment leads to the formation of colonic aberrant crypt foci (ACF). We have used these end-points to identify potential chemopreventive agents that might be effective against heterocyclic amine colon carcinogens. Typically, IQ or PhIP were administered to groups of 10-15 rats by oral gavage on alternating days in weeks 3 and 4, and ACF were scored after 8, 12, or 16 weeks or tumors were detected at 52 weeks. To distinguish between 'blocking' and 'suppressing' agents, potential inhibitors were administered during the initiation or post-initiation phases, respectively, and subsequent studies focused on the inhibitory mechanisms. Among the most effective inhibitors identified to date, and their major mechanisms, were the following: chlorophyllin (molecular complex formation); indole-3-carbinol (inhibition and induction of cytochromes P450 and phase II enzymes); green and black tea catechins (induction of UDP-glucuronosyl transferase, inhibition of NADPH-cytochrome P450 reductase, scavenging of reactive intermediates); and conjugated linoleic acids (inhibition of cytochrome P450 and prostaglandin H synthase.

Porphyrins as possible preventers of heterocyclic amine carcinogenesis.
Hayatsu H, Sugiyama C, Arimoto-Kobayashi S, Negishi T.

Faculty of Pharmaceutical Sciences, Okayama University, Tsushima, Japan. hayatsu@ph2ews1.okayama-u.ac.jp

Our studies have shown that hemin and chlorophyllin can directly interact with heterocyclic amines (HAs) and prevent their mutagenic actions. Hemin and chlorophyllin can trap HAs efficiently, probably by forming face-to-face complexes with them. The trapping was most clearly demonstrated by use of solid-supported porphyrins, hemin-agarose and chlorophyllin-chitosan. Furthermore, spectroscopic measurements have suggested that there are interactions in solution between the porphyrins and the HAs. A number of in vivo data have been accumulated by efforts from many laboratories for the anticarcinogenic and antigenotoxic properties of porphyrins, particularly chlorophyllin, against HAs.
 

Inhibition of dibenzo[a,l]pyrene-induced multi-organ carcinogenesis by dietary chlorophyllin in rainbow trout.

Reddy AP, Harttig U, Barth MC, Baird WM, Schimerlik M, Hendricks JD, Bailey GS.

Department of Environmental Toxicology, Oregon State University, Corvallis, OR 97331, USA.

Cancer chemoprevention by dietary chlorophyllin (CHL) was investigated in a rainbow trout multi-organ tumor model. In study 1, duplicate groups of 130 juvenile trout were treated for 2 weeks with control diet, 500 p.p.m. dibenzo[a,l]pyrene (DB[a,l]P) or 500 p.p.m. DB[a,l]P + 2052 p.p.m. CHL, then returned to control diet. DB[a,l]P alone proved somewhat toxic but induced high tumor incidences in liver (61%), stomach (91%) and swimbladder (53%) 11 months after initiation. CHL co-feeding abrogated DB[a,l]P acute toxicity and reduced tumor incidences to 18% in liver, 34% in stomach and 3% in swimbladder (P </= 0.01). A second tumor and DNA adduct study using a non-toxic initiation protocol (200 p.p.m. DB[a,l]P +/- 4000 p.p.m. CHL for 4 weeks) confirmed these results. Potential CHL inhibitory mechanisms were investigated. Dietary CHL inhibited hepatic DB[a, l]P-DNA adducts in the two tumor studies by 89 and 76%, respectively. CHL was shown to complex strongly with DB[a,l]P (K(d1,2) = 1.59 +/- 0.01 &mgr;M, stoichiometry 2CHL:DB[a,l]P) and strongly inhibited DB[a,l]P mutagenesis in the Salmonella assay. Significant inhibition occurred at CHL concentrations substantially less than stoichiometric with DB[a,l]P and thus not reflecting simple DB[a,l]P sequestration via complexation. These initial findings suggest that CHL chemoprevention reflects complexation that might limit DB[a,l]P uptake in vivo, antimutagenic mechanisms such as catalytic degradation of the proximate electrophile in target cells, or both. These results demonstrate that dietary CHL is a reproducibly effective chemopreventive agent for DB[a,l]P multi-organ tumorigenesis in trout and suggest that reduced DB[a,l]P-DNA adducts may be predictive biomarkers of CHL reduction of DB[a,l]P-initiated hepatic tumors.
 

Chlorophyllin as an effective antioxidant against membrane damage in vitro and ex vivo.

Kamat JP, Boloor KK, Devasagayam TP.

Cell Biology Division, Bhabha Atomic Research Centre, 400 085, Mumbai, India.

Chlorophyllin (CHL), the sodium-copper salt and the water-soluble analogue of the ubiquitous green pigment chlorophyll, has been attributed to have several beneficial properties. Its antioxidant ability, however, has not been examined in detail. Using rat liver mitochondria as model system and various sources for the generation of reactive oxygen species (ROS) we have examined the membrane-protective properties of CHL both under in vitro and ex vivo conditions. Oxidative damage to proteins was assessed as inactivation of the enzymes, cytochrome c oxidase and succinic dehydrogenase besides formation of protein carbonyls. Damage to membrane lipids was measured by formation of lipid hydroperoxides and thiobarbituric acid reactive substances. The effect of this compound on the antioxidant defense system was studied by estimating the level of glutathione and superoxide dismutase. ROS were generated by gamma-radiation, photosensitization, ascorbate-Fe(2+), NADPH-ADP-Fe(3+) and the peroxyl radical generating agent, azobis-amidopropane hydrochloride. Our results show that CHL is highly effective in protecting mitochondria, even at a low concentration of 10 microM. The antioxidant ability, at equimolar concentration, was more than that observed with ascorbic acid, glutathione, mannitol and tert-butanol. When CHL was fed to mice at a dose of 1% in drinking water, there was a significant reduction in the potential for oxidative damage in cell suspensions from liver, brain and testis. To examine the possible mechanisms responsible for the observed antioxidant ability we have studied the reaction of CHL with the potent ROS in the form of hydroxyl radical and singlet oxygen. The compound shows a fairly high rate constant with singlet oxygen, in the order of 1.3x10(8) M(-1) s(-1). In conclusion, our studies showed that CHL (Chlorophyllin) is a highly effective antioxidant, capable of protecting mitochondria against oxidative damage induced by various ROS.
 

Plants Provide Prevention

Worldwide, approximately 473,000 new cases of liver cancer are diagnosed annually, with 80% occurring in the developing world. Two risk factors work synergistically to greatly increase the risk of liver cancer: chronic infection with hepatitis B virus (HBV), which affects approximately 350 million individuals, and chronic exposure to aflatoxins, especially aflatoxin B1, highly potent liver toxicants produced by molds that contaminate dietary staples. Both risk factors are especially prevalent in the developing world, but one step toward reducing this threat may be chemoprevention, the use of drugs or dietary supplements to derail aflatoxin exposure effects. In a study published in the 4 December 2001 issue of Proceedings of the National Academy of Sciences, scientists found that chlorophyllin, an artificially produced water-soluble salt of the plant pigment chlorophyll, shows promise as such a chemopreventive agent.

Thomas Kensler, a professor of environmental health sciences at the Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland, directed the chlorophyllin trial. He says a two-pronged approach is needed to combat the problem: HBV vaccination--the most important part--for the viral component, and chemoprevention for the aflatoxin component. "Since there is this multiplicative interaction between the chemical and the virus, if either one can be knocked down, there can be a pretty dramatic impact, at least in theory, on cancer burden," he says.

As a step toward proving that theory and to test the efficacy of chlorphyllin as a chemopreventive agent, researchers looked to the Chinese city of Qidong, where liver cancer is the leading cause of cancer death and accounts for up to 10% of all adult deaths in some rural townships. The researchers recruited 180 individuals from villages near Qidong, all of whom had demonstrable aflatoxin exposure but were healthy. They were randomly assigned to take either a placebo or a 100 mg dose of chlorophyllin three times daily, 20 minutes before each meal, for 16 weeks.

The key finding came from urine samples collected in week 12. These samples revealed a significant decrease in urinary aflatoxin-N7-guanine, a biomarker of aflatoxin-induced DNA damage, in the treated group compared to the placebo group. The level of this biomarker allows researchers to assess chemoprevention efficacy. In the Qidong trial, participants who received chlorophyllin had approximately half as much urinary aflatoxin-N7-guanine as those in the placebo group. A study published by University of Washington researcher Lawrence A. Loeb in the 15 April 2001 issue of Cancer Research suggests that reducing aflatoxin-induced DNA damage by this margin might delay liver cancer development for decades.

Chlorophyllin's mechanism of action is still unclear, but there is some indication that it attaches to the aflatoxin, thereby impeding absorption and shuttling the toxin through the digestive tract. Kensler says other mechanisms may be involved as well. What makes chlorophyllin especially attractive is that it's inexpensive and safe. There were no side effects reported by the study group other than darker-than-normal stool. The sole drawback appears to be the number of times the treatment must be taken each day.

According to Kensler, the next question is whether chlorophyllin can reduce the incidence of liver cancer itself. "We're taking tentative steps to moving in that direction, but that's a major undertaking so we want to make sure we know exactly how to [design and conduct the study] to [get] the best likely outcome," he says.

"Chlorophyllin is certainly a promising chemopreventive compound for aflatoxin exposure reduction, given the dramatic effects seen on DNA damage levels observed in the Chinese study," say Paul Turner and Christopher Wild, molecular epidemiologists at the University of Leeds School of Medicine in Great Britain, whose own research has focused on the HBV-aflatoxin relationship and alternative aflatoxin intervention approaches in West Africa.

Although HBV vaccination will have the greatest influence on reducing liver cancer incidence, Turner and Wild emphasize that addressing the problem of aflatoxin exposure is also important. Aflatoxin exposure itself probably contributes to the incidence of liver cancer independently of HBV infection, they say, and vaccination will provide no protection for the millions who already carry the virus. In addition, say the researchers, "despite World Health Organization recommendations, economic and logistic problems result in only one percent of children in Africa currently having access to HBV vaccination. For these groups of people, aflatoxin exposure intervention could significantly reduce their liver cancer risk."

Use of aflatoxin adducts as intermediate endpoints to assess the efficacy of chemopreventive interventions in animals and man.

Kensler TW, Groopman JD, Roebuck BD.

Department of Environmental Health Sciences, Johns Hopkins School of Hygiene and Public Health, Baltimore, MD 21205, USA. tkensler@jhsph.edu

Clinical cancer prevention studies that use disease as an endpoint are of necessity, large, lengthy, and extremely costly. Development of the field of cancer chemoprevention is being accelerated by the application of intermediate markers to preclinical and clinical studies. Sensitive and specific analytic methods have been developed for detecting and quantifying levels of covalent adducts of aflatoxins with cellular DNA and blood proteins at ambient levels of exposure. Such biomarkers can be applied to the preselection of exposed individuals for study cohorts, thereby reducing study size requirements. Levels of these aflatoxin-DNA and albumin adducts can be modulated by chemopreventive agents such as oltipraz and chlorophyllin in experimental models. Overall, a good concordance is seen between diminution of biomarkers and reductions in tumor incidence and/or multiplicity in these settings. Thus, these markers can also be used to rapidly assess the efficacy of preventive interventions. However, the successful application of these biomarkers to clinical prevention trials will be dependent upon prior determination of the associative or causal role of the marker to the carcinogenic process, establishment of the relationship between dose and response, and appreciation of the kinetics of adduct formation and removal. The general approach that has been utilized for the development, validation and application of aflatoxin-DNA and protein adduct biomarkers to cancer chemoprevention trials is summarized. Copyright 1998 Elsevier Science B.V. All rights reserved.

Chlorophylls:
Can These Green Food Pigments
Prevent Some Cancers? 

George S. Bailey, Ph.D.
Distinguished Professor of Food Toxicology
OSU/LPI Affiliate Investigator

Chlorophyll, the natural plant pigment that lends its color to grass, leaves, and many of the vegetables we eat, may play an important role in prevention of certain cancers. Researchers in the early 1980s discovered that chlorophylls and related chemicals can inhibit the ability of certain DNA-damaging chemicals to cause mutations in bacteria. How might this kind of "anti-mutagenic" activity be important in cancer prevention? Molecular geneticists now know that most if not all human cancers carry mutations in one or more genes that control the rates at which individual cells divide, differentiate, or die. According to current thinking, various combinations of mutations that upset this delicate balance to favor uncontrolled cell growth can then enable this irreversibly damaged cell to form a primary cancer in the lung, liver, blood, bone, skin, or another body organ. Therefore, it seems at least theoretically possible that the anti-mutagenic power of the chlorophylls might allow them to inhibit or reduce the formation of cancers in humans. Recent progress in our laboratory and elsewhere has brought this promise closer to realization.

People in certain parts of Africa, China, and other developing countries with similarly warm, damp climates have the highest rates of liver cancer in the world. The two major risk factors are chronic hepatitis B viral infection, and exposure to aflatoxin B1 (AFB1) in the food supply. People exposed to both factors are at extremely high risk for liver cancer. Peanuts, corn, rice, and other grains and nuts stored under warm damp conditions can be infected with the mold Aspergillus flavus, which produces AFB1 as a secondary metabolite. AFB1 is one of the most potent cancer-causing chemicals, or carcinogens, ever discovered. Interestingly, AFB1 came to be recognized as a potential human liver carcinogen only after it was identified as the cause of outbreaks of liver cancer in rainbow trout hatcheries in the Pacific Northwest in the 1960s. Much of that pioneering work was carried out at Oregon State University by Professor Russel Sinnhuber who immediately recognized the promise of the rainbow trout as a model of exquisite sensitivity for the study of liver cancer. Postdoctoral fellows and graduate students in my laboratory have been using this model for the past 12 years in a search for means to reduce AFB1-based liver cancer risk. Dr. Roderick Dashwood, a postdoctoral associate who came to my lab in 1986, became interested in chlorophylls. Although their anti-mutagenic activity in bacterial assays was then well known, no one knew if chlorophylls could have a protective effect in animals. Rod discovered that rainbow trout fed AFB1 together with chlorophyllin, a simple water-soluble chlorophyll derivative, had greatly reduced damage to their liver DNA compared to trout receiving AFB1 alone. Would this reduce liver cancer development? That question was answered by a Ph.D. student, Vibeke Breinholt, who showed that even very modest dietary levels of chlorophyllin, roughly equivalent to the chlorophyll in one small helping of spinach, strongly reduced liver cancer in trout co-fed AFB1. Vibeke's results also showed clearly that this reduction could be directly attributed to reduced AFB1-DNA damage in the liver. These very exciting findings were the first ever to reveal a true cancer-protective effect by chlorophylls. Several important questions now remained before these findings might be taken to human trials: Was the effect unique to trout or would chlorophyllin inhibit cancer in other animals? How did the cancer inhibition come about and would this mechanism likely apply to AFB1-exposed humans? Could chlorophyllin inhibit cancers other than liver or caused by carcinogens other than AFB1 -- that is, might it have a potentially broader applicability? Would native chlorophylls in the plants we eat be as effective as the chlorophyllin derivative? The answers to most of these questions are now known. Rod Dashwood, presently at University of Hawaii, found that chlorophyllin in the drinking water could strongly reduce colon cancer development in rats exposed to heterocyclic amines, which are potent carcinogens isolated from meats broiled at high temperature. Others found similar protection against skin tumors in mice painted with polyaromatic hydrocarbons, and we have shown protection against stomach and liver cancer in trout treated with a carcinogenic hydrocarbon found in tobacco smoke. Subsequent work by Vibeke, Michael Schimerlik, and Tetsu Hayashi showed that chlorophyllin associated tightly with AFB1, even in the acidic environment of the stomach and at the temperature of the human body, which most likely explained the ability of chlorophyllin to greatly reduce bioavailability or uptake of AFB1 from the diet. John Groopman and Tom Kensler two colleagues at Johns Hopkins University, found that dietary chlorophyllin was as effective at preventing AFB1-DNA damage in the liver of rats as it was in trout. Such a simple and safe protective mechanism was almost sure to apply to humans! Based on these findings and the known safety of chlorophyllin, the National Institute of Environmental Health Sciences recently funded a research grant for Drs. Kensler, Groopman, and me to conduct a chlorophyllin intervention trial in a region of China where people are unavoidably exposed to high levels of AFB1 in their diet. In August I ventured to the little town of Daxin where Tom and I, with the help of local physicians from the Qidong Liver Cancer Institute, initiated the trial. After screening 500 volunteers, over 200 people were identified with high levels of chronic AFB1 exposure. Of these, 90 people will receive a green sugar pill and 90 will receive a green chlorophyllin tablet with each meal for four months. (The samples are all coded and nobody knows who gets what until the code is revealed at the very end). Blood and urine samples are being collected every second week. By analysis of these samples we hope to tell if chlorophyllin alters AFB1 uptake and liver DNA damage in people as it does in trout and rats. The experiment can detect a reduction of 20% or greater, and, of course, this is what we hope to see. On a personal note, those of us trained in the basic sciences rarely have an opportunity to see our work applied directly to the reduction of human disease and misery. It would be rewarding indeed to see the trout model applied full circle from the discovery of a major form of human cancer risk, to the discovery of a simple means for its prevention. By this time next year I hope to be able to tell you how this turns out.   The Outcome Follows 11.28.01 Chlorophyllin Reduces Aflatoxin Indicators Among People At Risk For Liver Cancer A study conducted by researchers at the Johns Hopkins Bloomberg School of Public Health shows that taking chlorophyllin greatly reduces the levels of aflatoxin-DNA damage byproducts in the body, which are indicators of exposure to carcinogenic aflatoxins and increased risk of liver cancer. Chlorophyllin is a derivative of chlorophyll and is used as an over-the-counter diet supplement and as a food colorant. The results appear in the November 27, 2001 edition of Proceedings of the National Academy of Sciences. “Our study shows that taking chlorophyllin three times a day reduced the amounts of aflatoxin-DNA damage by 55 percent, compared with taking a placebo,” says Thomas Kensler, PhD, professor of environmental health sciences at the Johns Hopkins Bloomberg School of Public Health. “Taking chlorophyllin or eating green vegetables, like spinach, that are rich in chlorophyll may be a practical way of reducing the risk of liver cancer and other cancers caused by environmental triggers,” explains Dr. Kensler. Dr. Kensler and his colleagues conducted a double-blind study among residents of Qidong, China. The people of the region have an extraordinarily high rate of liver cancer, which is due in part from routinely eating foods contaminated with carcinogenic aflatoxins. The aflatoxin is produced by molds found in foods like corn, peanuts, soy sauce, and fermented soybeans. For the study, researchers recruited 180 healthy adults. Half of the group was given 100 mg tablets of chlorophyllin to take three times a day with meals for four months. The other half was given a placebo. Urine and blood samples were taken over four months to determine the effects of chlorophyllin on excretion of aflatoxin-DNA damage products. According to the study’s results, the people who took chlorophyllin showed a 55 percent reduction in aflatoxin-DNA damage, compared to the placebo group. “Studies conducted by our co-author, George Bailey of Oregon State University, have suggested that chlorophyllin acts as an ‘interceptor molecule’ to block the absorption of aflatoxins and carcinogens in the diet,” explains John Groopman, PhD, professor and chairman of the Department of Environmental Health Sciences at the Johns Hopkins Bloomberg School of Public Health. “Our study shows that chlorophyllin can effectively reduce aflatoxin levels, which should reduce the risk of liver cancer. Since chlorophyllin is found in many foods or can be easily added to the diet, it could be a safe and effective prevention method. The study adds to the evidence that green vegetables contain effective anticarcinogens,” adds Dr. Groopman. Follow up studies are planned to determine whether this early protective action of chlorophyllin extends to either delay the onset or reduce the incidence of liver cancer. Patricia Egner, Jin-Bing Wang, Yuan-Rong Zhu, Bao-Chu Zhang, Geng-Sun Qian, Shuang-Yuan Kuang, Stephen J. Gange, Lisa P. Jacobson, Kathy J. Helzlsouer, George S. Bailey, John D. Groopman, and Thomas W. Kensler assisted in the research and writing of the article “Chlorophyllin intervention reduces aflatoxin-DNA adducts in individuals at high risk for liver cancer.” The study was funded by grants from the U.S. Public Health Service, National Institute of Environmental Health Sciences. Note: This story has been adapted from a news release issued for journalists and other members of the public. If you wish to quote any part of this story, please credit Johns Hopkins University Bloomberg School Of Public Health as the original source.