Chronic fluoride toxicity and myocardial damage: Antioxidant offered protection in second generation rats

Abstract

This experiment was designed to investigate the extent of peroxidative changes and histological alterations in the myocardium of rats exposed to high fluoride for two generations, in addition to ameliorative role of selenium and vitamin E on the above indices. Adult albino Wistar rats were given fluoride through drinking water (200 ppm F) and maintained subsequently for two generations, while they were exposed to fluoride throughout the experiment. Fluoride treatment significantly increased the lipid peroxidation and decreased the activity of antioxidant enzymes, viz., catalase, superoxide dismutase, and glutathione level in auricle and ventricle regions of the heart. Decreased feed and water consumption, organ somatic index and marginal drop in body growth rate were observed. Decreased antioxidant enzymes and increased malondialdehyde levels might be related to oxidative damage that occurs variably in the myocardium of rats. Biochemical changes were supported by the histological observations, which also revealed that chronic exposure to fluoride causes damage to the myocardium. Results of this study can be taken as an index of cardio-toxicity in rats exposed to water fluoridation. Further, oral supplementation of selenium and vitamin E not only inhibited oxidative stress but also enhanced the activities of antioxidant enzymes. Administration of antioxidants during fluoride exposure significantly overcame cardiac fluoride toxicity and therefore may be a therapeutic strategy for fluorotic victims.

Epigallocatechin gallate potentially attenuates Fluoride induced oxidative stress mediated cardiotoxicity and dyslipidemia in rats

“…TNF-␣ acts as a major mediator in the pathogenesis of cardiac injury, promoting inflammation, apoptosis and accumulation of extracellular matrix. Several studies have shown the higher levels of inflammatory cytokines, such as TNF-␣, IL-1␤, and IL-6 are involved in processes leading to cardiac remodelling such as hypertrophy, fibrosis, and apoptosis [61]. In our study, we found that TNF-␣-level was increased from the heart tissue of F intoxicated rats clearly indicates the cardiac inflammation, which coincides with the reports of Nabavi et al [9] in F intoxicated rats.…”

Sodium Fluoride Induces Apoptosis in H9c2 Cardiomyocytes by Altering Mitochondrial Membrane Potential and Intracellular ROS Level

“…However, more and more evidence showed that fluoride intoxication produces oxidative stress and damages various tissues [25][26][27][28]. The cardiovascular systems are susceptible to a high concentration of fluoride, because many cardiovascular dysfunctions have been observed, such as the decreasing of cardiac output, the occurrence of arrhythmias, and heart block [7,8,29]. However, the mechanisms of fluorosis in the cardiovascular system need to be further illustrated.…”

“…Fluorine is an active nonmetallic element, which easily interacts with calcium and magnesium in the blood, thus causing blood calcium metabolism disorder, leading to the functional and organic damage to the cardiovascular and other systems [6]. Studies showed that fluoride has severe detrimental effects on cardiac function in atherosclerosisrelated myocardial injury and pathophysiological remodeling [7][8][9][10][11]. However, very few studies have ever addressed the mechanism of action of fluorosis in cardiovascular system.…”

Is water fluoridation a hidden cause of obesity? Histological study on thyroid follicular cells of albino rats

“…It is also known to cause damage to major organs of the body including the heart and the gastrointestinal tract. Its accumulation in soft tissues causes injury by reducing the potential of scavenging free radicals production, which critically injures the biological membranes [5]. It also intensifies free radical production and a disturbed antioxidant level leads to oxidative stress, which is known to be a key etiopathological factor in a variety of cardiac diseases [6,7].…”