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

Azab, Azab Elsayed; Albasha, Mohamed Omer; Jbireal, JM; Adwas, Almokhtar A.

doi:10.4236/ojapo.2018.71001

Cited by 18 publications

(8 citation statements)

References 43 publications

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“…In our study, NaF caused testes oxidative damage, as demonstrated by lower antioxidant enzyme (Cat, SOD and GPx) levels in the NaF‐treated group. The findings of our investigation were consistent with the findings of a number of other studies that found NaF to be toxic to testes, liver, and kidney tissues [21,22] . In the current study, supplementing NaF‐treated rats with HES kept the levels of the above‐mentioned destruction markers in their testes tissues at normal levels.…”

Section: Resultssupporting

confidence: 92%

Contribution of Oxidative Stress, Apoptosis, Endoplasmic Reticulum Stress and Autophagy Pathways to the Ameliorative Effects of Hesperidin in NaF‐Induced Testicular Toxicity

Kızıl¹,

Gür²,

Ayna³

et al. 2023

Chemistry & Biodiversity

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The ameliorative effects of hesperidin (HES) on the toxicities created by sodium fluoride (NaF) in the testes tissue of rats were studied via oxidative stress, apoptosis and endoplasmic reticulum (ER) stress pathways. The animals were divided into five distinct groups (7 rats in each group). Group 1 was control group, group 2 received NaF-only (600 ppm), group 3 received HES-only (200 mg/kg bw); group 4 received NaF (600 ppm) + HES (100 mg/kg bw) and group 5 received NaF (600 ppm) + HES (200 mg/kg bw) for 14 days. NaF-induced testes tissue damage by reducing activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) and levels of glutathione (GSH), and increasing lipid peroxidation levels. NaF treatment significantly downregulated the mRNA levels of SOD1, CAT and GPx. NaF supplementation caused apoptosis in the testes by upregulating p53, NFkB, caspase-3, caspase-6, caspase-9, and Bax and downregulating Bcl-2. Furthermore, NaF caused ER stress via increasing mRNA transcript levels of PERK, IRE1, ATF-6 and GRP78. NaF treatment led to autophagy via upregulation of Beclin1, LC3A, LC3B and AKT2. In testes tissue, however, co-treatment with HES at doses of 100 and 200 mg/kg significantly reduced oxidative stress, apoptosis, autophagy and ER stress. Overall, the findings of this study suggest that HES may help to reduce testes damage caused by NaF toxicity.

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Section: Resultssupporting

confidence: 92%

Contribution of Oxidative Stress, Apoptosis, Endoplasmic Reticulum Stress and Autophagy Pathways to the Ameliorative Effects of Hesperidin in NaF‐Induced Testicular Toxicity

Kızıl¹,

Gür²,

Ayna³

et al. 2023

Chemistry & Biodiversity

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“…Moreover, the fluoride toxicity was found to cause a significant increase in aminotransferase activity, as reported in cattle (37) and in goat (38), so these elevations could be due to a secondary event following SF induced LPO of hepatocyte membranes with the subsequent increase in the leakage of these biomarkers from the liver tissue (39). However, an increase of apoptosis is consequent to the exposure of fluoride, had been reported in various mammalian cells (40 and 41) as well as, the increase in the cytochrome C release from mitochondria and the activation of both the intrinsic and extrinsic pathway of cell death have been reported in SF exposure (42), which was accompanied with a decrease in the antioxidant status of liver leading to impairment of its function (43). The hepatoprotective activity of PSO was reflected via a decrease in the ALT and AST levels in group T2 as compared with SF treated rats and returned to normal range.…”

Section: Resultsmentioning

confidence: 94%

Effect of Pomegranate Seed Oil against Hepatotoxicity- Induced by Sodium Fluoride in Adult Female Rats (Part II).

Al-Okaily¹

2019

Iraqi J. Vet. Med.

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This experiment was designed to evaluate the hepatoprotective effects of pomegranate seed oil against toxicity- induced by sodium fluoride and in normal rats. Twenty adult female Wistar rats were divided into four equal group and treated daily for 40 days as follows: Group C administered tap water and served as control , group T1 : received sodium fluoride 120ppm in drinking tap water, group T2: received both sodium fluoride 120ppm in drinking water and administered orally pometone (pomegranate seed oil) 30mg/kg B.W. and group T3 : administered pomegranate seed oil as in group T2 orally. Fasting blood samples were collected at 0, 20 and 40 days to estimation of some biochemical parameters and oxidative stress biomarkers . In addition, sections from liver were taken at the end of the experiment for histopathological study. The results revealed that SF (group T1) caused a significant increase in serum aminotransferases (serum alanine aminotransferase and aspartate aminotransferase) activities, total cholesterol ,total bilirubin and peroxynitrite radical concentrations, while GSH concentration was a significantly decrease. PSO caused an alleviation to the hepatic dysfunction induced by sodium fluoride (group T2) manifested through significant elevation of GSH concentration, in addition, a significant reduction in serum transaminases activity, total cholesterol, peroxynitrite radical and total bilirubin concentrations. In contrast, administration of pomegranate seed oil (group T3) showed no alterations in most of these parameters. Furthermore histopathological examination of liver tissues of group T1 manifested aggregation of mononucleated cells, proliferation of hepatocyte, cytoplasmic fat droplet and granulomatous lesion consists of aggregation of macrophage and lymphocyte. All these alteration in liver histology were modified by treatment of rats with pomegranate seed oil (group T2) and no pathological lesion was reported in group T3. On conclusion, this study documented the beneficial effect of pomegranate seed oil against the deleterious effects of SF on liver functions of adult female rats.

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“…These findings are basically in agreement with the results obtained from similar investigations by Liang et al (1999). In addition, plasma creatinine concentration is a more sensitive indicator than urea in the first phases of kidney disease; more seriously, the higher level of urea and creatinine in blood might be due to an inability of kidney to excrete the toxic metabolic product (Azab, Albasha, Jbireal, & Adwas, 2018). In addition, fluoride and aluminum possess a higher capacity to cross cell membranes and easily, inter-visceral organs especially brain, liver, and kidney, as consequences, are burdened with the high levels of these elements (Abdel Aziz & Masad, 2013;Wasana, Perera, Gunawardena, & Bandara, 2015).…”

Section: Discussionmentioning

confidence: 99%

Potential toxicity of aluminum and fluoride on some biochemical aspects of male rat’s offspring

Kinawy

2019

JoBAZ

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Background: This work was designed to evaluate the potential hazards of sodium fluoride (NaF) and aluminum chloride (AlCl 3) given separately or in conjugation throughout the prenatal and up to weaning time or till the postnatal 70th day. The levels of the following parameters were then assessed; vitamin C (ascorbic acid), glutathione (GSH) and oxidized glutathione (GSSH), malondialdehyde (MDA), total protein, albumin, total calcium, ionized calcium, creatinine, urea, uric acid, and bilirubin. In addition, the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined. In this study, female pregnant rats were allocated into four groups. The first received the drinking deionized water and served as a normal group, the second was given a daily dose of NaF (0.15 g/L) dissolved in deionized water from day 6 of gestation till the end of the weaning period, and the third was given a daily dose of AlCl 3 (500 mg/L) for the same period of time. The fourth group was given drinking water containing combined doses of NaF + AlCl 3 for a similar length of time. Each group was further divided into two subgroups; the first continued to be treated with the same pollutants in drinking deionized water at the same dose level until the age of 70 days, whereas the second group was supplied with pure deionized water free from the intoxicating substances for the same period of time. Results: The results revealed that either NaF or AlCl 3 given separately or in conjunction with each other abated the quenching effects of the antioxidant system and induced oxidative stress and several perturbations in the aforementioned parameters. The metals caused significant increase in the levels of urea, uric acid, creatinine, and activities of ALT and AST activities, whereas the levels of total and ionized calcium in serum and the concentration of vitamin C, GSH, and GSH/GSSG ratio in hepatic tissues were significantly decreased and the levels of MDA were markedly increased in the liver as a response to the studied metals. Conclusion: Based on the present results, the exposure to sodium fluoride or aluminum chloride induced profound perturbation in the liver and kidney functions.

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

Cited by 18 publications

References 43 publications

Contribution of Oxidative Stress, Apoptosis, Endoplasmic Reticulum Stress and Autophagy Pathways to the Ameliorative Effects of Hesperidin in NaF‐Induced Testicular Toxicity

Contribution of Oxidative Stress, Apoptosis, Endoplasmic Reticulum Stress and Autophagy Pathways to the Ameliorative Effects of Hesperidin in NaF‐Induced Testicular Toxicity

Effect of Pomegranate Seed Oil against Hepatotoxicity- Induced by Sodium Fluoride in Adult Female Rats (Part II).

Potential toxicity of aluminum and fluoride on some biochemical aspects of male rat’s offspring

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