Liver cancer is the fifth most common cancer in men and the ninth in women. An estimated 782,500 new liver cancer cases occurred in the world during 2012, with China alone accounting for about 50% of the total. Rates are more than twice as high in men as in women. Liver cancer rates are the highest in Central America, West and Central Africa, and East and Southeast Asia.
Aflatoxins are among the most potent mutagenic and carcinogenic substances known. Differential potency of aflatoxin among species can be partially attributed to differences in metabolism; however, current information on competing aspects of metabolic activation and detoxification of aflatoxin in various species does not identify an adequate animal model for humans. Risk of liver cancer is influenced by a number of factors, most notably carriage of hepatitis B virus as determined by the presence in serum of the hepatitis B surface antigen (HBsAg+ or HBsAg-). About 50 to 100% of liver cancer cases are estimated to be associated with persistent infection of hepatitis B (or C) virus.
The potency of aflatoxin in HBsAg+ individuals is substantially higher (about a factor of 30) than the potency in HBsAg- individuals. Thus, reduction of the intake of aflatoxins in populations with a high prevalence of HBsAg+ individuals will have greater impact on reducing liver cancer rates than reductions in populations with a low prevalence of HbsAg+ individuals. The present analysis suggests that vaccination against hepatitis B (or protection against hepatits C), which reduces prevalence of carriers, would reduce the potency of the aflatoxins in vaccinated populations and reduce liver cancer risk.
This research has led to potential chemopreventative strategies for liver cancer in populations at high risk for aflatoxin exposure. “Aflatoxin is a very lipid soluble molecule so that when we ingest it, it’s rapidly absorbed. And it goes first to the liver where there are enzymes that will chemically biotransform it into a very reactive chemical, which attacks with very high preference, our DNA, causing damage to that DNA, mutations, perhaps in genes that enhance our susceptibility to cancer production. Aflatoxin is also a very cytotoxic molecule so it will directly kill some of our liver cells creating a void, if you will, that causes the remaining liver cells to replicate and perhaps grow at a faster rate than we would like. The combination of DNA damage and cell proliferation triggers the liver cancer process.”
Mold-contaminated crops can be a serious problem especially in countries where proper storage facilities are limited.
Professor Kensler explains their clinical trials in which chlorophyllin was administered as a therapy and the resultant levels of aflatoxin DNA damage products present in urine samples.
It has been estimated that the DNA in each cell of the body suffers 10,000 oxidative hits per day, leading to the formation of more than 20 different oxidative DNA lesions.108 Human studies show lifestyle and other environmental influences may profoundly modify outcomes of aging.109,110
It is not just environmental toxins (e.g., cigarette smoke, coal dust, and diesel emission particles) that pose a concern. Foods cooked at high temperatures also inflict cellular damage. Deep-fried foods along with well-done beef steak, hamburgers, and bacon cause the formation of gene-mutating heterocyclic amines.111,112 Even so-called healthy foods contain small amounts of undesirable substances.113
Chlorophyllin has been shown to have DNA-protective and antioxidant properties, inhibiting DNA adduction.101,114-116 Chlorophyllin also quenches all major oxygen species and acts to protect mitochondria.117-119 Chlorophyllin also has a role in preventing unavoidable dietary exposure to aflatoxin, a naturally occurring mycotoxin, by reducing its oral bioavailability.120
Keywords: John Hopkins bloomberg school of public health, liver toxicity, environmental health sciences, food and drug administration, liver cancer, aflatoxin, grain product, school of public health, hepatitis b, strict guidelines, department of agriculture, biomarkers, carcinogen, metabolite, food supply, byproduct