Oxidative stress responses as a marker of toxicity in mice exposed to polluted groundwater from an automobile junk market in South-Western Nigeria.

The global trade in used vehicles and their components generates huge financial benefits but leads to detrimental environmental consequences including groundwater pollution and potential adverse health effects mediated by free-radical processes such as lipid peroxidation. We investigated oxidative stress responses in thirty-six, female mice orally exposed (via drinking) to graded concentrations (0%, 50%, and 100%) of groundwater from a well located within a major automobile junk market in SW-Nigeria containing extremely high levels of arsenic (0.332 ± 0.089 mg/l) and seventeen PAHs, which serves as domestic water supply. Blood samples from the mice were assayed for selected biochemical parameters at intervals of 7, 14, and 28 days. A significant dose- and duration-dependent increase in malondialdehyde (MDA) and Myeloperoxidase (MPO) confirmed oxidative stress onset due to exposure to the polluted well-water, while a significant decline in nitric oxide (NO-) levels may suggest impaired endothelial smooth-muscle relaxation which may lead to the development of metabolic diseases over time. Superoxide dismutase (SOD) and reduced glutathione (GSH) showed a contrasting trend with Glutathione peroxidase (GPx), while Glutathione-S-Transferase (GST) declined significantly by the 28th day. Two clusters were identified by principal component analysis-one involving MDA, SOD, and GSH suggesting that antioxidant responses driven mainly by SOD and GSH proved insufficient in scavenging the free radicals generated by lipid peroxidation. NO- and total protein clustered together possibly due to the significant declines in both over the study period. Histological examination of liver tissue of exposed mice corroborated the above findings and highlights the need for urgent remedial action.