Prevention of Mercury-Induced Cardiotoxicity After Short-Term Egg White Hydrolysate Supplementation in Rats

Mercury exposure triggers localized oxidative stress, playing a central role in its detrimental effects, because toxic levels of ROS induce lipid peroxidation, promote protein oxidation and nitration, and nucleic acid oxidation and damage. Egg white hydrolysate (EWH), a functional food, is a protein extract that has promising capabilities against metal-induced cardiovascular damage. However, its potential in preventing the acute effects of mercury exposure remains unexplored. This study evaluated the preventive efficacy of 3 days, a short-term EWH treatment against the subsequent acute exposure to HgCl₂ in isolated left ventricle papillary muscles. Male Wistar rats were divided into four groups: Control, EWH, HgCl₂ and EWH + HgCl₂. Animals received filtered water or EWH (1 g/kg/day) via oral gavage for 3 days as pre-treatment. Subsequently, papillary muscles were isolated, and then HgCl₂ and EWH + HgCl₂ groups were exposed to 6 nM HgCl₂ for 60 min. Results revealed that acute HgCl₂ exposure impaired force generation, positive and negative time derivatives of force, indicating contractile dysfunction. Notably, these effects were absent in the EWH + HgCl₂ group. Furthermore, HgCl₂ exposure depressed post-rest potentiation, inotropic response protocols to calcium and isoproterenol while the EWH + HgCl₂ group exhibited comparable responses to the control group. Besides that, the increase in ROS levels induced by HgCl₂ in vitro was prevented by EWH pre-treatment. In conclusion, EWH demonstrated a cardioprotective effect by preserving contractile function, maintaining physiological inotropic responses, and preventing ROS accumulation with a remarkably brief 3-day pre-treatment period, highlighting its potential against the deleterious effects of acute mercury exposure, particularly in unavoidable or unpredictable exposures.