Prophylactic effect of N-acetylcysteine against sodium fluoride-induced blood oxidative stress in mice

Altıntaş, Levent; Eşsiz, Dinç; Eraslan, Gökhan; İnce, Sinan; Arslanbaş, Emre

doi:10.1016/j.fct.2010.07.015

Cited by 14 publications

(7 citation statements)

References 38 publications

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“…CAT is responsible for the breakdown of hydrogen peroxide and protects the tissues from the potential toxicity of hydroxyl radicals [ 51 ]. Consequently, the effects of SOD and CAT are complementary to each other [ 54 ]. In this study, it was found that the SOD and CAT activities were decreased in the 24 and 48 mg/kg groups, suggesting that the superoxide radicals and/or hydroxyl radicals were accumulated in the kidney.…”

Section: Discussionmentioning

confidence: 99%

Histopathological findings of renal tissue induced by oxidative stress due to different concentrations of fluoride

et al. 2017

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It has been reported that excessive intake of fluoride can induce renal lesions. However, its pathogenesis is still less understood. Therefore, this study was conducted to investigate oxidative damage and the relationships between the oxidative damage and renal lesions in fluoride-treated mice by using the methods of histopathology, biochemistry, flow cytometry and quantitative real-time polymerase chain reaction (qRT-PCR). A total of 240 ICR mice were randomly divided into four equal groups (sodium fluoride was given orally at the dose of 0, 12, 24 and 48 mg/kg body weight for 42 days, respectively). We found that fluoride in excess of 12 mg/kg induced renal oxidative damage, which was characterized by increasing the levels of reactive oxygen species (ROS) production and contents of malondialdehyde (MDA) and protein carbonyls (PC), and decreasing the abilities of anti-superoxide anion (ASA) and anti-hydroxyl radical (AHR), glutathione (GSH) content, as well as activities and mRNA expression levels of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione peroxidase (GSH-Px). Concurrently, fluoride caused degeneration and necrosis of the tubular cells, renal tubular hyaline casts and glomeruli swelling, which were consistent with the alteration of renal function parameters including elevated contents of serum creatinine (Cr), serum uric acid (UA), blood urea nitrogen (BUN), and the activities of urinary N-acetyl-b-D-glucosaminidase (NAG), renal lactate dehydrogenase (LDH), and reduced activities of sodium-potassium adenosine triphosphatase (Na+/K+-ATPase) and acid phosphatase (ACP) in the kidney. The above-mentioned results showed that fluoride in excess of 12 mg/kg induced renal oxidative damage, which then caused renal lesions and dysfunctions. These findings also clearly demonstrated that oxidative damage is one of the mechanisms of fluoride-induced renal lesions and dysfunctions.

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Section: Discussionmentioning

confidence: 99%

Histopathological findings of renal tissue induced by oxidative stress due to different concentrations of fluoride

et al. 2017

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“…Antioxidant defense systems, including non-enzymatic and enzymatic antioxidant systems, can scavenge oxidative radicals from oxidative injuries. It was suggested that antioxidants (such as vitamins, methionine, N-acetyl-cysteine; polyphenolic flavonoids) and antioxidant-rich foods (such as blackberry juice) can act as antidotes for the management of fluorosis [25,26,27,28,29]. …”

Section: Discussionmentioning

confidence: 99%

Maize Purple Plant Pigment Protects Against Fluoride-Induced Oxidative Damage of Liver and Kidney in Rats

Zhang

Zhou

Wang

et al. 2014

IJERPH

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Anthocyanins are polyphenols and well known for their biological antioxidative benefits. Maize purple plant pigment (MPPP) extracted and separated from maize purple plant is rich in anthocyanins. In the present study, MPPP was used to alleviate the adverse effects generated by fluoride on liver and kidney in rats. The results showed that the ultrastructure of the liver and kidney in fluoride treated rats displayed shrinkage of nuclear and cell volume, swollen mitochondria and endoplasmic reticulum and vacuols formation in the liver and kidney cells. MPPP significantly attenuated these fluoride-induced pathological changes. The MDA levels in serum and liver tissue of fluoride alone treated group were significantly higher than those of the control group (p < 0.05). The presence of 5 g/kg MPPP in the diet reduced the elevation of MDA levels in blood and liver, and increased the SOD and GSH-Px activities in kidney and GSH level in liver and kidney compared with the fluoride alone treated group (p < 0.05). In addition, MPPP alleviated the decrease of Bcl-2 protein expression and the increase of Bax protein expression induced by fluoride. This study demonstrated the protective role of MPPP against fluoride-induced oxidative stress in liver and kidney of rats.

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“…Fluorides can injure the endothelial barrier; furthermore, they modulate the inflammatory response and cellular migrations (Bogatcheva et al , 2006; Barbier et al , 2010). Previous studies of changes in adhesion molecule expression resulting from the exposure to fluorides were sparse (Bohnet et al , 1994; Zhang et al , 2007; Altintas et al , 2010; Bian et al , 2010; Chen et al , 2010). The evidence that oxidative stress can affect the processes of intercellular adhesion and that fluorides can impair the pro‐oxidant–antioxidant balance of cells suggests a potential mechanism by which fluorides can modulate adhesion molecule expression.…”

Section: Discussionmentioning

confidence: 99%

Effects of fluorides on apoptosis and activation of human umbilical vein endothelial cells

2011

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Prophylactic effect of N-acetylcysteine against sodium fluoride-induced blood oxidative stress in mice

Cited by 14 publications

References 38 publications

Histopathological findings of renal tissue induced by oxidative stress due to different concentrations of fluoride

Histopathological findings of renal tissue induced by oxidative stress due to different concentrations of fluoride

Maize Purple Plant Pigment Protects Against Fluoride-Induced Oxidative Damage of Liver and Kidney in Rats

Effects of fluorides on apoptosis and activation of human umbilical vein endothelial cells

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