Contamination with mercury is a real health issue for humans with physiological consequences. The main objective of the present study was to assess the neurotoxicological effect of inorganic mercury: HgCl2. For this, adult mice were exposed prenatally, postnatally, and during the adult period to a low level of the metal, and their behavior and antioxidant status were analyzed. First, we showed that mercury concentrations in brain tissue of treated animals showed significant bioaccumulation, which resulted in behavioral deficits in adult mice. Thus, the treated mice developed an anxiogenic state, as evidenced by open field and elevated plus maze tests. This anxiety-like behavior was accompanied by a decrease in social behavior. Furthermore, an impairment of memory in these treated mice was detected in the object recognition and Y-maze tests. The enzymatic activity of the antioxidant system was assessed in eight brain structures, including the cerebral cortex, olfactory bulb, hippocampus, hypothalamus, mesencephalon, pons, cerebellum, and medulla oblongata. The results show that chronic exposure to HgCl2 caused alterations in the activity of catalase, thioredoxin reductase, glutathione peroxidase, superoxide dismutase, and glutathione S-transferase, accompanied by peroxidation of membrane lipids, indicating a disturbance in intracellular redox homeostasis with subsequent increased intracellular oxidative stress. These changes in oxidative stress were concomitant with a redistribution of essential heavy metals, i.e., iron, copper, zinc, and magnesium, in the brain as a possible response to homeostatic dysfunction following chronic exposure. The alterations observed in overall oxidative stress could constitute the basis of the anxiety-like state and the neurocognitive disorders observed.
