Fluoride Action Network


Fluoride contamination in drinking water due to natural and anthropogenic activities has been recognized as one of the major problems worldwide imposing a serious threat to human health. Excessive exposure to fluoride appears to be serious and causes metabolic, functional and structural damages in many organs especially in the heart. Calcium is a chelating agent for fluoride and can reduce its toxicity. This study was conducted to investigate some of the toxic effects of sodium fluoride (NaF) on albino rats heart and the role of Ca administration on these toxic changes. Thirty adults’ male albino rats were used in this study. The animals were divided into five groups (6 animals each); Group I (-ve control), given standard diet and tape water, Group II: (+ve control) received 0.1 mL distilled water/ day by oral gavage. Group III: received calcium chloride at a dose 20 mg/kg b.wt./day. Group IV: received sodium fluoride treatment (NaF) at a dose 20 mg/kg b.wt./day. Group V: animals given sodium fluoride (NaF) at a dose 20 mg/kg/day and calcium chloride given 4 hours after NaF treatment at a dose of 20 mg/kg/day. The duration of the study was 28 days. The rats then were anesthetized and blood was collected for estimation of troponin T, Lactate dehydrogenase (LDH) and creatine phosphokinase (CPK). The hearts were saved for light and electron microscopic examinations. The results revealed that NaF induced cardio toxicity which reflected in significant increase in troponin T, LDH and CPK. Light microscopic examination of the heart of NaF treated rats showed marked distortion of the myocardial structure including rupture of the muscle fibers, widening of the intercellular space and massive inter-myofibrillar hemorrhage, appearance of cytoplasmic vacuoles, peripheral displacement of its nuclei. There was also dilatation and congestion of the blood capillaries and lymphocytic infiltration in the inter-myofibillar spaces. Electron microscopic examination revealed, irregularities of the nuclear membrane with increase of the heterochromatic patches. The cytoplasm showed swelling of the mitochondria, rupture of the cell membrane of some cardiomyocytes and extravasations of cell organelles in the intercellular space. There was also thinning of the myofibrils that appeared attenuated with marked discontinuity of the intercalated discs. The cytoplasm also contained many vacuoles. In rats treated with NaF and Ca significant decrease in troponin T, LDH and CPK were observed compared to those treated with NaF only. The myofibrils retained its arrangement with few fibers are still thinned with rounded and flat nuclei and areas of cellular distortion. There were also areas of lymphocytic infiltration. The nuclei showed enfolding of its nuclear membrane, thick patches of heterochromatin and numerous nucleoli. It was concluded that NaF is a cardio-toxic agent and these toxicities could be minimized by concomitant use of Ca. It was recommended that exposure to F should be regulated and Ca supplement is better to be received to minimize its side effects.