Chronic exposure to electronic waste poses risk to liver toxicity with molecular interaction of GSTM1, GSTT1 null variants, and GSTP1.

Chronic exposure to electronic waste (e-waste) is becoming a serious concern for health among individuals exposed to it. E-waste has been reported to contain heavy metals, trace elements, and persistent organic pollutants which can trigger health issues through different biological pathways. The liver is a major metabolic and detoxifying organ in the body. Glutathione S-transferase (GST) is a liver enzyme for phase II detoxification that catalyzes glutathione (GSH) conjugation with environmental pollutants. This research aimed to investigate the liver toxicity caused by long-term exposure to e-wastes, exploring the potential association with null variants of GSTT1 and GSTMI, as well as GSTP1. The study was designed as a cross-sectional investigation, in which 256 adult males who were chronically exposed to e-waste and 200 non-exposed control participants, matched for age and gender, were recruited randomly. Standard colorimetric and enzymatic methods were used to analyze biochemical parameters such as serum alkaline phosphatase (ALP), alanine transaminase (ALT), total bilirubin (T. Bil), albumin, and reduced glutathione. Genotypic analysis of the null variant GSTM1, GSTT1, and GSTP1 genes was conducted by standard molecular methods. The study findings indicated a notable surge in ALP, ALT, and albumin levels while T. Bil and GSH levels showed a reduction, suggesting a potential risk of liver toxicity. Additionally, analysis of GSTM1, GSTT1, and GSTP1 genotypes revealed a possible association with GSH levels and the hepatotoxicity risk. The study concluded that the individuals exposed to e-waste exhibited dysregulation of liver enzymes that results in liver toxicity. Moreover, analysis of GSTM1, GSTT1, and GSTP1 at a molecular level revealed that these genes could potentially serve as risk factors for liver toxicity in e-waste chronic exposure.