Abstract
AFB1 and MC-LR are two major environmental risk factors for liver damage worldwide, especially in warm and humid areas, but there are individual differences in health response of the toxin-exposed populations. Therefore, we intended to identify the susceptible genes in transport and metabolic process of AFB1 and MC-LR and find their effects on liver damage. We selected eight related SNPs that may affect liver damage outcomes in AFB1 and MC-LR exposed persons, and enrolled 475 cases with liver damage and 475 controls of healthy people in rural areas of China. The eight SNPs were genotyped by PCR and restriction fragment length polymorphism. We found that SLCO1B1 (T521C) is a risk factor for liver damage among people exposed to high AFB1 levels alone or combined with MC-LR, and that GSTP1 (A1578G) could indicate the risk of liver damage among those exposed to high MC-LR levels alone or combined with high AFB1 levels. However, GSTP1 (A1578G) could reduce the risk of liver damage in populations exposed to low MC-LR levels alone or combined with high AFB1 levels. In conclusion, SLCO1B1 (T521C) and GSTP1 (A1578G) are susceptible genes for liver damage in humans exposed to AFB1 and/or MC-LR in rural areas of China.
Highlights
Aflatoxins, HBV and microcystins are three risk factors for liver cancer in the world
For the other six SNPs, SLCO1B3 (T334G), GSTT1 (−/+), GSTM1 (−/+), GSTA1 (C69T), CYP2E1 (C1019T) and cytochrome P450 3A4 (CYP3A4) (A13871G), we found no statistical differences in cases and controls of the target population (Supplementary material)
These results suggested that the risk of liver damage may be associated with SLCO1B1 (T521C) and GSTP1 (A1578G) among people exposed to AFB1 or/and MC-LR for a long time
Summary
Aflatoxins, HBV and microcystins are three risk factors for liver cancer in the world. The metabolism of aflatoxin is mainly through liver[3,4], and the major human cytochrome p450 enzymes involved in its www.nature.com/scientificreports/. AFB1 is metabolized to a reactive epoxide (aflatoxin-8,9-epoxide, AFBO) catalyzed by CYP1A2 and CYP3A4 in humans[5,6]. In humans and most animals, the major route of AFB1 detoxification is via conjugation of AFBO to endogenous GSH by the classical detoxification glutathione S-transferases (GSTs)[10]. We deduced that the gene polymorphism of transport and metabolic pathways of AFB1 and MC-LR could affect the transport and metabolism of the two toxins, leading to differences in the individual sensitivity among AFB1 and MC-LR exposed populations
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