The wide range of adverse effects caused by aflatoxin assumption is named aflatoxicosis and has been reported in two forms:
(i) “acute intoxication” caused by short exposure to great amount of toxins and characterized by severe liver damage, jaundice, haemorrhage, oedema and eventually death; and
(ii) “chronic sublethal exposure,” which leads to immunosuppression, nutritional dysfunctions and cancer.
Among these toxins, Aflatoxin B1 (AFB1) is considered the most recurrent and also the most harmful. Its carcinogenicity and immunosuppression capacity have been extensively reported in all kind of animals, including Poultry، trout، cattle and rats with different incidence across species, gender and age.
Several in vitro studies demonstrated that the carcinogenicity of AFB1 is prevalently exerted upon activation by Cytochromes P450 (CYP450) in the liver and elucidated the mechanism of its toxicity.
Another toxin causing great concern is Aflatoxin M1 (AFM1), the principal hydroxylated metabolite of AFB1, found in milk (hence the designation M) of mammals fed upon contaminated feedstuff.
Carry-over of AFB1 as AFM1 in the milk of dairy cows has been established to range from 0.3% to 6.2% . However, AFM1 was also found in lactating mother’s milk. Several studies reported carcinogenic and immunosuppressive effects، similar to that of AFB1, on both humans and other animals, even if with a less potent effect
Aflatoxins are fungal metabolites found in feeds and foods. When the ruminants eat feedstuffs containing Aflatoxin B1 (AFB1), this toxin is metabolized and Aflatoxin M1 (AFM1) is excreted in milk. International Agency for Research on Cancer (IARC) classified AFB1 and AFM1 as human carcinogens belonging to Group 1 and Group 2B, respectively, with the formation of DNA adducts. In the last years, some epidemiological studies were conducted on cancer patients aimed to evaluate the effects of AFB1 and AFM1 exposure on cancer cells in order to verify the correlation between toxin exposure and cancer cell proliferation and invasion. In this review, we summarize the activation pathways of AFB1 and AFM1 and the data already reported in literature about their correlation with cancer development and progression. Moreover, considering that few data are still reported about what genes/proteins/miRNAs can be used as damage markers due to AFB1 and AFM1 exposure, we performed a bioinformatic analysis based on interaction network and miRNA predictions to identify a panel of genes/proteins/miRNAs that can be used as targets in further studies for evaluating the effects of the damages induced by AFB1 and AFM1 and their capacity to induce cancer initiation.
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