Sublethal Doses of Inorganic Mercury Induce Dose-Depended Upregulation of RPA1 Content and Inhibit p53 Expression in the Brain of Rainbow Trout (Oncorhynchus mykiss)

Mercury (Hg) is one of most toxic and widespread element of aquatic environment. Almost every kind of the fish can accumulate Hg. Hg-induced peculiarities of cellular malfunction could be used as adequate biomarker to estimate the contamination risk in polluted aquatic ecosystems. The brain cells are high susceptible to the Hg compounds cytotoxicity. Various Hg species have different harmful effects on both structure and function of the brain cells. Neurotoxicity of inorganic Hg remains discussable and studied restrictedly. In this study, we have studied the role of RPA1 and p53 proteins in brain cell response to sublehtal (25% LD50 and 50% LD50) doses of inorganic Hg in rainbow trout (Oncorhynchus mykiss). LD50 value of Hg chloride in presented study was determined as 551 μg/L relate to 96 hours exposure. Two sublethal doses were used in the exposure rainbow trout at 2 and 7 days. The treatment with Hg chloride induced in fish brain dose-dependent increase in ROS level as well as time-dependent growth. Moreover, the exposure to both 25% and 50% LD50 Hg doses have caused significant upregulation of RPA1 expression. In the brain tissue of fish exposed to Hg for 2 days, it stimulated slightly expression of p53. Contrary, 7 days exposure induced significant decrease in p53 expression. The results of presented study evidence that sublethal doses of inorganic Hg are extremely neurotoxic and can induce in the fish brain signaling pathways disturbance through decline of stress sensor protein p53. Besides, the increase in RPA1 expression let to assume that brain cells of the fish can repair ROS-induced DNA breaks and prevent genotoxic effect of inorganic Hg. Overall, current data pointed out that inorganic mercury is high toxic to fish brain cells and this question requires future research