Liver - Adverse Effects
Sodium fluoride
CAS No. 7681-49-4

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• Note: The following is a limited selection of abstracts from 1994 to present.
• Due to length, we present this as a separate section
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Liver section for fluorine & organofluorine pesticides.
• When time allows more information will be added.

J Inorg Biochem 2003 Jan 15;93(3-4):243-6.

Substrate inhibition of rat liver and kidney arginase with fluoride

Tormanen CD.

Department of Chemistry, Central Michigan University, Mount Pleasant, MI 48858, USA.

Abstract: Fluoride is an uncompetitive inhibitor of rat liver arginase. This study has shown that fluoride caused substrate inhibition of rat liver arginase at substrate concentrations above 4 mM. Rat kidney arginase was more sensitive to inhibition by fluoride than liver arginase. For both liver and kidney arginase preincubation with fluoride had no effect on the inhibition. When assayed with various concentrations of L-arginine, rat kidney arginase did not have Michaelis-Menten kinetics. Lineweaver-Burk and Eadie-Hofstee plots were nonlinear. Kidney arginase showed strong substrate activation at concentrations of L-arginine above 4 mM. Within narrow concentrations of L-arginine, the inhibition of kidney arginase by fluoride was uncompetitive. Fluoride caused substrate inhibition of kidney arginase at L-arginine concentrations above 1 mM. The presence of fluoride prevented the substrate activation of rat kidney arginase.

Lik Sprava 2002 Apr-Jun;(3-4):104-6.

[Article in Russian]

[Features of the effects of zinc and fluorine on functional status of rat liver]

Inoiatov FSh.

Abstract: Intoxication of rats of both sexes three months in duration leads to development of cytolysis and hepatocellular insufficiency, with females displaying a higher degree of it. At the same time, fluorine promotes development of hypolipoperoxidation in males. In females, unlike males, intensification of LPO tended to grow higher and was to be seen with both agents. SOD activation has been revealed in exposure of females to zinc and of males to both fluorine and zinc. Also revealed in the animals was activation of catalase, especially so in males. Activation of membranodestructive processes in the liver of test animals brings about a decline in the pharmacometabolizing function of the organ.

Fluoride 2002; 35(3):153-160.

Brain lipid peroxidation and antioxidant systems of young rats in chronic fluoride intoxication.

Shivarajashankara YM et al.

Abstract: Summary: A study was made of the effect of fluoride on oxidative stress in rats during their early stages in life. Wistar albino rats were exposed to 30 ppm and 100 ppm fluoride (from sodium fluoride) in drinking water during the last one week of intrauterine life and then up to ten weeks after birth...
-- Excerp ... Increased free radical generation and lipid peroxidation are proposed to mediate the toxic effects of fluoride on soft tissues (10-12). Earlier, we reported increased lipid peroxidation and disturbed antioxidant defense systems in brain, erythrocytes and liver of rats exposed to high-fluoride intake during the stages of life after weaning (13). There is, however a paucity of studies on the effect of fluoride intoxication during the early developing stages of life on oxidative stress. Recently, we observed increased lipid peroidation and altered levels of antioxidants in the blood of children with endemic skeletal fluorosis (14) and in the liver of young rats exposed to high levels of fluoride in drinking water during the early stages of life (15)...

Full report available at

Fluoride 2001; 34(2):108-113.

Effect of fluoride intoxication on lipid peroxidation and antitoxidant systems in rats;

YM Shivarajashankara, AR Shivashankara, P Gopalakrishna Bhat, S Hanumanth Rao.

Abstract: SUMMARY: The effect of fluoride intoxication on lipid peroxidation and anti-oxidant systems in the blood, brain, and liver of rats was studied. Twelve one-month-old albino rats were administered 100-ppm fluoride (as NaF) in their drinking water for four months. In the red blood cells the levels of malondial-dehyde (MDA) and glutathione (GSH) increased, along with the activity of glutathione peroxidase (GSH-Px), but the activity of superoxide dismutase (SOD) decreased. In the plasma the level of ascorbic acid increased while that of uric acid decreased. In the brain and liver, MDA and GSH levels increased, as did the activities of GSH-Px and glutathione S-transferase (GST). The level of ascorbic acid increased in the brain, but it decreased in the liver. These results suggest that fluoride enhances lipid peroxidation in the red blood cells, brain and liver of rats and causes increased or decreased enzyme activity associated with free radical metabolism.

Full report available at

Fluoride 2001; 34(1):34-42.

Histopathology of fluoride-induced hepatoxicity in rabbits

A Shashi and SP Thapar.

Abstract: SUMMARY: The effect of chronic and acute exposure to sodium fluoride (5, 10, 20, and 50 mg/kg body weight/day) for fifteen weeks on hepatic damage in young albino rabbits was evaluated. Histopathological examination revealed increasing degrees of hepatocellular necrosis, degenerative changes, hepatic hyperplasia, extensive vacuolization in hepatocytes, and centrilobular necrosis in the liver of the exposed animals. The central vein and sinusoids of the liver were dilated and engorged with blood and were associated with small areas of haemorrhages. These effects were not observed in the control group.

Full report available at

Fluoride Vol. 33 No. 1 6-16 2000

Liver Morphology and histochemistry in rats resulting from ingestion of Sodium selenite and Sodium fluoride

L Kolodziejczyk (a), A Put (b), P Grzela (b)

(a) For correspondence: Department of Biology and Medical Parasitology, Pomeranian
Medical University, 70-111 Szczecin, al. Powsta n´ ców Wielkopolskich 72, Poland.
(b) Department of Toxicology, Pomeranian Medical University, Szczecin, Poland.

Abstract: SUMMARY: A morphological and histochemical assessment was made of the effect of sodium selenite and sodium fluoride on oxidative and lysosomal enzyme activity in the liver of male rats. The compounds were administered separately and together for a period of three months. Oxidative enzyme activity of a-glycerophosphate dehydrogenase (a -GlDH) and succinate dehydrogenase (SDH) increased with sodium selenite and decreased with sodium fluoride
and with both compounds together. Sodium selenite in a dose of 1 0 µg/kg body weight and sodium fluoride in a dose of 20 mg/kg body weight caused an increase in the activity of acid phosphatase (AcP), while the combined dose caused a decrease in the activity of this enzyme.

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