Niacin prevents mitochondrial oxidative stress caused by sub-chronic exposure to methylmercury

Abstract

Humans and animals can be exposed to different chemical forms of mercury (Hg) in the environment. For example, methylmercury (MeHg)-contaminated fish is part of the basic diet of the riparian population in the Brazilian Amazon Basin, which leads to high total blood and plasma Hg levels in people living therein. Hg induces toxic effects mainly through oxidative stress. Different compounds have been used to prevent the damage caused by MeHg-induced reactive oxygen species (ROS). This study aims to investigate the in vivo effects of sub-chronic exposure to low MeHg levels on the mitochondrial oxidative status and to evaluate the niacin protective effect against MeHg-induced oxidative stress. For this purpose, Male Wistar rats were divided into four groups: control group, treated with drinking water on a daily basis; group exposed to MeHg at a dose of 100 µg/kg/day; group that received niacin at a dose of 50 mg/kg/day in drinking water, with drinking water being administered by gavage; group that received niacin at a dose of 50 mg/kg/day in drinking water as well as MeHg at a dose of 100 µg/kg/day. After 12 weeks, the rats, which weighed 500-550 g, were sacrificed, and their liver mitochondria were isolated by standard differential centrifugation. Sub-chronic exposure to MeHg (100 µg/kg/day for 12 weeks) led to mitochondrial swelling (p < 0.05) and induced ROS overproduction as determined by increased DFCH oxidation (p < 0.05), increased gluthatione oxidation (p < 0.05), and reduced protein thiol content (p < 0.05). In contrast, niacin supplementation inhibited oxidative stress, which counteracted and minimized the toxic MeHg effects on mitochondria.

Nicotinic Acid against Acetaminophen-Induced Hepatotoxicity via Sirt1/Nrf2 Antioxidative Pathway in Mice

“…In this research, we mainly explored the role of NA on antioxidant stress in APAP-induced liver injury, In fact, evidences suggest that supplementation of NA protected male C57BL/6 mice from hepatocytes deaths and alcohol-induced liver injury by reducing oxidative stress in a protein kinase B (Akt) dependent manner (23). NA also inhibited mitochondrial oxidative stress evoked by methylmercury (MeHg) poisoning in male Wistar rats (24). Other scholars reported that dietary NA administration was sufficient to resist oxidative damage in rat liver under tert-butyl hydroperoxide challenge and improved hepatic zinc uptake as well (25).…”

Mercury and Alzheimer’s Disease: Hg(II) Ions Display Specific Binding to the Amyloid-β Peptide and Hinder Its Fibrillization

“…The Hg-induced disruption of the ROS defense [88] likely promotes the ROS-related component of AD pathology [94,98]. This might be particularly relevant for the mitochondria, as they are often affected by Hg exposure [165,166], and as mitochondrial dysfunction is commonly observed in AD brain neurons [62,[167][168][169].…”

Stress management in aquaculture: a review of dietary interventions

“…Riboflavin (vitamin B 2 ) and niacin (Nicotinamide/nicotinic acidvitamin B 3 ) are also known to possess potent antioxidant properties both independently and also as components of the glutathione redox cycle (Ganji et al 2009;Ashoori & Saedisomeolia 2014;Ilkhani et al 2016;Marashly & Bohlega 2017) and modulate immune functions in fish (Chen et al 2015b;Sharifzadeh et al 2015;Feng et al 2016;Li et al 2016b;Mohammadi et al 2019;Xun et al 2019). Recently, dietary administration of niacin ameliorated methyl mercury-induced oxidative stress and genotoxicity in rats (de Paula et al 2016;Pereira et al 2020). Therefore, dietary inclusion of niacin seems to be an efficient approach to mitigate the adverse effects of stress in fish.…”