Effects of sodium fluoride on total serum protein levels and transaminase activity in rats

Qujeq, Durdi; Laghaie, B; Gholipour, Afshin; Solimani, N; Hassenzadeh, S

doi:10.1016/s0753-3322(02)00172-5

Cited by 10 publications

(4 citation statements)

References 8 publications

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“…They added that, during the secretory process, incompletely assembled and aggregated products were selectively retained in the rER. Qujeq et al [31] reported that fluoride inhibited protein synthesis.…”

Section: Discussionmentioning

confidence: 99%

The Possible Protective Role of Methionine against Sodium Fluoride-Induced Pancreatic Changes in the Adult Male Albino Rat: A Histological, Immunohistochemical and Morphometric Study

Zaghloul

Gad-Elrab

Bushra

et al. 2019

Egyptian Journal of Histology

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Background: Excess fluorides intake produces histopathological changes of many organs. Methionine is a potential natural antioxidant against oxidative radicals. Aim of the Work: To evaluate the possible protective role of methionine against sodium fluoride (NaF)-induced pancreatic toxicity. Material and Methods: Thirty 3-months (200-250gm) adult male albino rats were divided into three equal groups: group I (control), group II (Fluoride group) and group III (Fluoride+methionine group). Control group; was given 1ml distilled water. Fluoride group; was given 10 mg NaF/kg b.w. Fluoride+methionine group; was given 10 mg NaF/kg b.w. and 2 mg methionine/rat. All the treatment was given orally by gastric tube once daily for 35 days. After anesthesia, all groups were sacrificed. The pancreatic specimens were prepared for light and electron microscopic studies and anti-insulin antibody immunohistochemical staining. The mean numbers of zymogen granules and insulin positive β-cells of all groups were counted. Results: The mean numbers of zymogen granules and insulin positive β-cells of the fluoride group were significantly decreased when compared to control. The pancreatic specimens of the fluoride group revealed congested blood vessels, extravasated blood cells, vacuolated pancreatic acini, loss of the acinar cell architecture, dilated rough endoplasmic reticulum and degenerated mitochondria. By anti-insulin antibodies immunohistochemistry, there was a weak positive reactivity in the fluoride treated group when compared to control. The concomitant administration of NaF and methionine improved these changes. Conclusion: The concurrent administration of NaF and methionine ameliorates the structural alterations developed in the pancreas following excess NaF intake.

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Section: Discussionmentioning

confidence: 99%

The Possible Protective Role of Methionine against Sodium Fluoride-Induced Pancreatic Changes in the Adult Male Albino Rat: A Histological, Immunohistochemical and Morphometric Study

Zaghloul

Gad-Elrab

Bushra

et al. 2019

Egyptian Journal of Histology

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“…Liver cells contain more AST than ALT, but ALT is confined to the cytoplasm in which its concentration is higher than that of AST [19]. Fluoride toxicities caused elevated in the activities of transaminases in rats and mice [42,43].…”

Section: Discussionmentioning

confidence: 99%

Potential Protective Effects of Blackberry and Quercetin on Sodium Fluoride-inducedImpaired Hepato-renal Biomarkers, Sex Hormones and Hematotoxicity in Male Rats

Ismail

Hamza

El-Shenawy

2014

JALSI

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Aim: The present study was carried out to evaluate the potential protective role of blackberry juice (BBJ) and quercetin (Q) against sodium fluoride-induced liver damage and impairment of kidney function, as well as hematotoxicity in rats. Study Design: After 2 weeks of acclimation, animals were divided into seven groups, ten rats each. All the groups were treated interaperitoneal (i.p.) for 30 successive days. Group 1 served as untreated control and received 1ml/Kg of distilled water i.p. daily. Group 2 was given i.p. BBJ at a dose of 1.6g/kgb.wt. containing 5mg anthocyanin. Group 3 was given quercetin at dose of 75mg/Kgb.wt. Group 4 was treated with 10.3mg/kg b.wt of NaF. Group 5 was given i.p. BBJ followed by NaF at the same doses. Group 6 was given quercetin followed by NaF and finally group 7 was treated with BBJ and Q then followed by NaF as mentioned previous doses. Methodology: Some hematological parameters were determined. Serum aspartate transaminase, alanine transaminase and alkaline phosphatase activities were as well as Original Research Articlelipid profile and total protein were evaluated as biomarkers for liver functions. The levels of uric acid and creatinine in serum were estimated. Hormones of testosterone and inhibin B were assessed. Results: Sodium fluoride (NaF) caused an elevation in serum transaminases and alkaline phosphatase and reduced serum total protein, testosterone, and inhibin-B levels as well as levels of uric acid and creatinine, and induced hematotoxicity. It increased all the parameters of lipid profile except the high density lipoprotein cholesterol level was decreased. The presence of Q or BBJ with NaF successfully mitigated liver and kidney functions, which was more pronounced with Q. Conclusion: It can be concluded that concomitant administration of Q or BBJ with NaF may be useful in reversing the toxicity of NaF in male rats.

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“…Fluoride toxicosis caused elevated in the activities of transaminases [6] [24] [34]. Also, Chattopadhyay et al, [35] reported that low (15 mg NaF/L) and relatively high (150 mg NaF/L) doses of in vivo fluoride treatment to Swiss albino mice through drinking water caused a disturbance in the liver function.…”

Section: B 2 Effect Of Sodium Fluoride On the Liver Functionmentioning

confidence: 99%

Sodium Fluoride Induces Hepato-Renal Oxidative Stress and Pathophysiological Changes in Experimental Animals

Azab¹,

Albasha²,

Jbireal³

et al. 2018

OJApo

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The liver is a primary site for xenobiotics detoxification, and its metabolism is readily altered by toxicity. The kidney is a common target for toxic xenobiotics due to its capacity to extract and concentrate toxic substances by highly specialized cells. So, they are the target organs of sodium fluoride toxicity. The aim of this review is to highlight on hepatorenal oxidative stress and pathophysiological changes induced by treatment of experimental animals with sodium fluoride. Our review shows fluoride toxicosis caused an elevation in the serum activities of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase, acid phosphatase, and the level of total bilirubin, and reduction in the serum levels of total protein, albumin, and globulins, and serious histopathological changes in the hepaic tissues. Also, NaF administration caused increases in serum urea, creatinine, uric acid, sodium ions, and chloride ions levels and serious histopathological changes in the kidney tissues. Treatment of experimental animals with NaF induced oxidative stress in hepatic and renal tissues. It can be concluded that administration of sodium fluoride to experimental animals induced oxidative stress, serious hepatorenal histopathological changes, and disturbance in liver and kidney functions. So, human should be advised to decrease exposure to sodium fluoride to decrease the harmful effects of NaF on liver and kidney.

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Effects of sodium fluoride on total serum protein levels and transaminase activity in rats

Cited by 10 publications

References 8 publications

The Possible Protective Role of Methionine against Sodium Fluoride-Induced Pancreatic Changes in the Adult Male Albino Rat: A Histological, Immunohistochemical and Morphometric Study

The Possible Protective Role of Methionine against Sodium Fluoride-Induced Pancreatic Changes in the Adult Male Albino Rat: A Histological, Immunohistochemical and Morphometric Study

Potential Protective Effects of Blackberry and Quercetin on Sodium Fluoride-inducedImpaired Hepato-renal Biomarkers, Sex Hormones and Hematotoxicity in Male Rats

Sodium Fluoride Induces Hepato-Renal Oxidative Stress and Pathophysiological Changes in Experimental Animals

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