Chronic exposure to methylmercury adversely affects response to oxidative stress.

Abstract

Methylmercury (MeHg) is an environmental neurotoxicant that has been shown to lead to physiological inefficiencies. Environmental contamination is a major concern, due to the high amounts of mercury pollution that affects a variety of food webs. Chronic exposure to MeHg has been shown to lead to the generation of reactive oxygen species (ROS) and inhibition of cell defense systems. The specific activities of three antioxidant enzymes, thioredoxin reductase (TrxR), glutathione peroxidase (GPx), and glutathione reductase (GR) are altered after chronic exposure to MeHg. Prior studies have shown generally, after MeHg exposure, the activity of TrxR and GPx decrease, while GR activity increases. These data imply that the glutathione system upregulates in the presence of MeHg, compensating for the inhibited activity of TrxR. This current study used kinetic spectroscopic methods to measure the activity and concentration of TrxR, GPx, and GR in Fundulus Heteroclitus exposed to MeHg in food at a rate of 35% of body weight per day for 3.5 weeks. We hypothesized that chronic exposure to MeHg lowers the activities of TrxR and GPx, and increases the activity of GR in brain and liver tissue. Results demonstrate that TrxR activity is unaffected after MeHg exposure in the liver of F. heteroclitus, whereas GPx and GR activity significantly decreased. Both TrxR and GPx activity decreased in the brain following MeHg treatment, while GR activity decreased only in males and remained unaffected in females. These findings provide insight into F. heteroclitus as an in vivo model for analyzing cellular responses to MeHg toxicity and how redox enzymes are affected by metal pollutants.