Protective effect of selenium against aluminium chloride induced cardiotoxicity in rats

Abstract

Materials and methodsChemicals Aluminium Chloride (AlCl3), selenium (Na2SeO3), glutathione (oxidized and reduced), AbstractOur study pertains to evaluate the protective effect of selenium (Se), used as a nutritional supplement, against aluminium chloride induced cardiotoxicity in rats. Rats have received during 21 days either AlCl3 (400 ppm) via drinking water, AlCl3 associated with Na2SeO3 (0.5 mg/kg of diet) or only Na2SeO3. Co-administration of Se to AlCl3 treated rats alleviated heart oxidative stress objectified by a decrease of malondialdehyde, hydrogen peroxide and protein carbonyls levels. An improvement in antioxidant redox status, enzymatic (catalase, superoxide dismutase and glutathione peroxidase) and non enzymatic (reduced glutathione, non protein thiols and vitamin C) was also observed in Se treated rats. LDH and CK activities, TC, LDL-C levels, TC/HDL-C and LDL-C/HDL-C ratios were increased, while HDL-C and TG decreased in rats treated with AlCl3. Cardiac biomarkers and lipid profile were restored to near control values by the supplementation of Se. Our results revealed that Se, a trace element with antioxidant properties, was effective in preventing heart damage induced by aluminium chloride.

Assessment of the Protective Effect ofLepidium sativumagainst Aluminum-Induced Liver and Kidney Effects in Albino Rat

“…In the present study, the significant disturbing effect of AlCl 3 administration on the lipid profile was evident as this was in agreement with previous studies of Ghorbel et al who reported that AlCl 3 induced abnormal activities of lipase enzymes that seem to be one of the chief factors responsible for the cholesterol rise in serum after AlCl 3 administration [4]. In an earlier study, Al-Hashem reported that the increased cholesterol and triglycerides induced by AlCl 3 indicated lost membrane integrity, disturbance of lipid metabolism, and/or liver dysfunction [27].…”

“…Oxidative stress is considered to be a major contributor, a trigger for sever metal toxicities, and has been reported to be associated with long retention of metals in some tissues [24]. It was well known that an imbalance between the overproduction of reactive oxygen species (ROS) and elimination of free radicals induces oxidative stress [4]. This study assessed the impact of AlCl 3 on the function and structure of the liver and kidney, the possible protective and therapeutic effects of LS against this impact, and the mechanism behind these effects.…”

“…The Agency for Toxic Substances and Disease Registry (ATSDR) reported that Aluminum is mainly distributed in the bone, liver, testis, kidneys, and brain [3]. This metal disrupts the prooxidant/antioxidant balance in tissues leading to biochemical and physiological dysfunctions due to an excessive reactive oxygen species (ROS) generation [4].…”

Histological study on the acute injection of aluminum sulfate on different organs of rats

“…The absence of histological abnormalities in the cardiomyocytes were detected after injection with Al 2 (SO 4 ) 3 even the significant increase of aluminum content in the heart of treated male and female rats with the highest dose. The obtained result is different from observed by Ghorbel, Elwej [31] who found that rats received AlCl 3 (400 ppm) for 21 days via drinking water induced cardiotoxicity. Novaes, Mouro [32] found that three highest doses of Al for 120 days induced heart toxicity and Gouda, El-Nabarawy [33] found that aluminium phosphide caused significant cardiac histopathological changes.…”

A conglomeration of preclinical models related to myocardial infarction

“…The exact mechanism of Al mediated toxicity is not yet been clear, but some correlates it with prooxidant properties of aluminium. With an end goal to enhance our comprehension on aluminium toxicity on heart mechanism, scientist have assessed the cardioprotective impact of selenium by overseeing aluminum chloride (50 mg/kg bw) for 21 days to deliver cardiotoxicity (Ghorbel et al, 2017).…”