Modulation of fluoride toxicity in rats by calcium carbonate and by withdrawal of fluoride exposure.
In order to assess the effect of calcium on the toxic effects of fluoride, adult female Wistar rats were treated with sodium fluoride (NaF, 500 ppm in drinking water) alone or in combination with calcium carbonate (CaCO3, 50 mg/ kg by oral intubation) daily for 60 days. Food, water and fluoride intake were measured daily for 60 days. Body weight gain, exploratory motor activity, rota-rod motor coordination, dental structure, activities of acetylcholinesterase (AchE, brain and skeletal muscle) and Na+ K+ ATPase (erythrocyte membrane and skeletal muscle) and the concentrations of protein (serum and skeletal muscle), calcium (serum) and fluoride (serum) were determined in these animals 24 hr after the last treatment. The same parameters were tested in another group, 60 days after withdrawal of NaF exposure (500 ppm in drinking water daily for 60 days). NaF treatment decreased food and water intake, reduced body-weight gain and impaired exploratory motor activity and rota-rod performance. Dental lesions, inhibition of the activities of AchE and N+ K+ ATPase and a decrease in the concentration of protein, and serum calcium were also observed in these animals. These effects were accompanied by a marked elevation of fluoride concentration in the serum. CaCO3 decreased the concentration of fluoride in the serum of NaF-treated animals. A decrease in serum fluoride concentration was found also after NaF withdrawal. A prevention of locomotor behavioural, biochemical and dental toxicities of fluoride was observed both in these groups. It is concluded that the dose of CaCO3 used in the present study has a potential to prevent the toxicity of fluoride by maintaining serum fluoride at a less toxic level. Further, the toxic effects of fluoride are reversible if its exposure is withdrawn for 2 months.
Ekambaram
P
P
Department of Pharmacology and Environmental Toxicology, Dr. A.L.M. Postgraduate Institute of Basic Medical Sciences, University of Madras, Taramani, Chennai, India. pgibms@md2.vsnl.net.in
Paul
Vanaja
V
D000110:Acetylcholinesterase / Q000378:metabolism; D000284:Administration, Oral; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects*; D001798:Blood Proteins / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D002119:Calcium Carbonate / Q000097:blood / Q000494:pharmacology*; D004910:Erythrocyte Membrane / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D005106:Exploratory Behavior / Q000187:drug effects; D005260:Female; D009043:Motor Activity / Q000187:drug effects; D009124:Muscle Proteins / Q000378:metabolism; D018482:Muscle, Skeletal / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012969:Sodium Fluoride / Q000097:blood / Q000633:toxicity*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
D001798:Blood Proteins; D009124:Muscle Proteins; D012969:Sodium Fluoride; D000110:Acetylcholinesterase; D000254:Sodium-Potassium-Exchanging ATPase; D002119:Calcium Carbonate