Protective effects of niacin against methylmercury-induced genotoxicity and alterations in antioxidant status in rats

Abstract

This study investigates the potential beneficial effects of niacin (NA; vitamin B3) supplementation in rats chronically exposed to methylmercury (MeHg). Animals were randomly assigned to one of 4 groups (n = 6): Group I, control, received distilled water by gavage; Group II, received MeHg (100 µg/kg/d) by gavage; Group III, received NA (50 mg/kg/d) in drinking water; Group IV, received MeHg (100 µg/kg/d) by gavage + NA (50 mg/kg/d) in drinking water. Biochemical parameters levels of glucose, triglycerides, total cholesterol and fractions, and enzyme activities aspartate transaminase (AST) and alanine transaminase (ALT) were determined. Further, oxidative stress markers activity of glutathione peroxidase (GPx) and catalase (CAT) activity, as well as levels of reduced glutathione (GSH), malondialdehyde (MDA), and nitric oxide, were examined, and the comet assay was performed, using blood/plasma. Hg levels were measured in blood, brain, and kidneys of animals. Our results demonstrated that NA reduced adverse effects produced by MeHg. The mechanism underlying these effects appears to be related to the intrinsic antioxidant potential of NA. Considering the beneficial effects attributed to NA following MeHg exposure and that fish are the main source of both NA and MeHg, future studies need to evaluate the potential counteractive effect of NA against the adverse consequences of MeHg exposure in fish-eating populations.

Biomarkers of mercury toxicity: Past, present, and future trends

“…These contradictory results are also inherent in animal studies. In rats Nath et al (1996) and more recently Silva de Paula et al (2016) noted no significant changes in CAT activity following exposure to Hg compounds, whereas Kong et al (2012) reported a decrease in activity levels during the embryonic development of a fish-model.…”

“…Due to the electrophilic nature of Hg, once absorbed into the organism, it binds nucleophilic groups, such as thiols (SH) and selenols (SeH) in cysteine (Cys) and selenocysteine (Sec), respectively. Consequently, peptides and proteins containing these moieties are targeted by mercurials (Carvalho et al, 2008a; Farina et al 2009; Rooney 2007; Silva de Paula et al, 2016).…”

“…In fact, GSH is present in some mammalian cells at concentrations as high as 10 millimolar (Cooper and Kristal, 1997) and Hg compounds (particularly, MeHg) were reported to induce oxidative damage in cultured cells when present at concentrations as low as 1 micromolar (Farina et al, 2009). In addition, experimental studies based on in vivo approaches noted reduced cerebellar (Franco et al, 2006), cerebral (Stringari et al, 2008) and blood (Silva de Paula et al, 2016) GSH levels in MeHg-exposed animals when Hg levels in these organs were in the low micromolar range. Thus, it is noteworthy that decreased GSH levels following Hg exposure do not necessarily indicate direct interaction between Hg and thiol groups, but may represent the consequence of direct oxidative effects of reactive species (i.e.…”

“…In fish exposed to MeHg no marked effect on SOD activity was found in liver and brain (Branco et al, 2011), whereas in brain of rats exposed to MeHg a significant increase in activity was observed (de Oliveira Souza et al, 2016). In the blood of rats chronically exposed to MeHg SOD activity remained unchanged relative to controls (Silva de Paula et al, 2016)…”

The effect of the germanium complex with nicotinic acid on oxidative modification of cardiac and hepatic proteins in the experimental chronic intoxication with doxorubicin in rats

“…Considering the pathological role of the oxidative stress in development of diseases and new data on the antioxidant properties of nicotinic acid [12,14] and efficacy of complex compounds of germanium with nicotinic acid [2][3][4] the aim of this work is to study POM in cardiomyocytes and hepatocytes under the effect of nicotinic acid and the complex compound of germanium with nicotinic acid (MIGU-1) synthesized for the first time in the laboratory of the Department of General Chemistry and Polymers of the I.I.Mechnikov Odessa National University under the supervision of professor I.Y.Seifullina on the model of chronic intoxication with doxorubicin (CID) in rats.…”