Abstract: Liver and kidneys are the important organs for metabolism, detoxification, homeostasis and excretion in most of the higher animals, including man. Toxic substances cause histopathological changes in both of these major tissues. Because the kidney get easily exposed to higher concentrations of fluoride than any other soft tissues ,excess fluoride exposure contributes to kidney damage, thus damaged kidneys increase the retention of fluoride, causing in turn further damage to the kidney, bone, and other organs. In animals, kidney damage has been reported at levels as low as 1 ppm if the animals consume fluoridated water for long periods of time. In the present investigation status of various membrane bound enzymes and other biochemicals in liver and kidney were studied in both control and experimental rats, which were given NaF in drinking water for 180 days. Acid phosphatase, LDH, and SDH were depleted significantly in liver after 180 days of fluoride feeding through drinking water. Alkaline phosphatase (P< 0.01), G-6-PD (P < 0.01) and ATPase (P< 0.01) were elevated significantly. GOT and GPT in liver were also increased significantly except GPT which was significant (P< 0.1) only in male rats .Significant (P< 0.1) decrease in liver proteins and elevated glycogen content were noted in all the experimental rats after 180 days of exposure to fluoride in drinking water. In kidney of experimental rats, alkaline phosphatase, GOT, GPT and ATPase were significantly elevated after chronic treatment of fluoride through drinking water. However, the enzymes acid phosphatase, LDH and SDH were significantly (P< 0.01) depleted. Total protein was found to be depleted significantly (60.07%) in male rats and 55.72% in female rats.
Keywords: Sodium Fluoride, Biochemical, Histo-pathological alterations, Soft Tissues, Liver, Kidneys, Wistar Albino Rat.
Title: Fluoride Induced Histo-pathological Alterations in Major Soft Organs of Wistar Albino Rat
Author: G. B. KALE
International Journal of Life Sciences Research
ISSN 2348-313X (Print), ISSN 2348-3148 (online)
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