Study of the protective effect of ascorbic acid against the toxicity of stannous chloride on oxidative damage, antioxidant enzymes and biochemical parameters in rabbits

Yousef, Mokhtar I.; Awad, T.I.; Elhag, F.A.; Khaled, Fayrouz A.

doi:10.1016/j.tox.2007.03.017

Cited by 44 publications

(33 citation statements)

References 41 publications

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“…Ascorbic acid is a non enzymatic antioxidant and is therefore potentially involved in protecting cells against oxidative stress. It also acts as a free radical scavenger and its presence assists various other mechanisms in decreasing numerous disruptive free radical processes (27). The co-administration of ascorbic acid with H 2 O 2 decreased lipid peroxidation.…”

Section: Discussionmentioning

confidence: 99%

“…The results indicate the beneficial effects of ascorbic acid to overcome oxygen dependent cytotoxicity in animals. Although the detail mechanism of the action of ascorbic acid is not fully understood, it is believed that the ascorbic acid as an anti oxidant might stimulate the 7-D-hydroxylation of lipids and cholesterol nuclei thus enhancing their degradation to bile acids, which could be excreted from the body (27,28). Vitamin C is an antioxidant, it possess substantial nucleophilic character and it has been suggested that, ascorbate might protect against electrophilic attack on cellular DNA and cell membranes by intercepting reactive agents (29) or that ascorbyl anion radical, with the high extent of unpaired electron delocalization, is responsible for the scavenging of free radicals or ascorbic acid might act as a chain breaking inhibitor of the peroxidation process by scavenging intermediary peroxyl and alkoxyl radical (30,31).…”

Section: Discussionmentioning

confidence: 99%

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Protective effect of ascorbic acid against oxidative damage induced by hydrogen peroxide in cultured human peripheral blood lymphocytes

Siddique

Beg

Afzal

2009

Indian J Clin Biochem

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Protective effect of ascorbic acid against oxidative damage induced by hydrogen peroxide in cultured human peripheral blood lymphocytes

Siddique

Beg

Afzal

2009

Indian J Clin Biochem

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“…In addition, vit. C increased the activities of GST, SOD and CAT, and the levels of SH-group and protein in stannous chlorideinduced oxidative damage (Yousef et al, 2007).…”

Section: Resultsmentioning

confidence: 88%

“…Since hyperammonemia results in increased utilization of (BCAAs) (Tomiya et al, 2002),treatment with α-LAC, a rich source of BCAAs (Morifuji et al, 2009), could facilitate ammonia detoxification by supporting muscle glutamine synthesis (Tomiya et al, 2002) while vit. C could counteract oxidative stress (Patra et al, 2001;Yousef et al, 2007;Mustafa et al, 2013). Groups treated with either α-LAC, vit.…”

Section: Resultsmentioning

confidence: 99%

Antioxidant and Hypo-Ammonemic Activities of Alpha-Lactalbumin and Vitamin C in Thioacetamide-Induced Liver and Brain Damage in Rats

Mansour¹,

Nada²,

Elmahmoudy³

et al. 2015

J App Pharm Sci

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Hepatic encephalopathy (HE) is a syndrome resulting from acute or chronic liver failure. The main hypothesis suggests a state of hyperammonemia which is responsible for both direct and indirect alterations in cerebral metabolism with increased production of reactive oxygen and nitrogen species. The effect of milk-derived alphalactalbumin (α-LAC) and vitamin C (vit. C) was evaluated in thioacetamide (TAA)-induced HEmodel in the current study. Animals were treated with TAA (100 mg/kg, i.p.) or saline thrice weekly for six weeks to induce HE then treatment groups received orally α-LAC (100 or150 mg/kg) and /or vit. C (500 mg/kg)daily for two weeks. Twenty-four hours after last treatment sera, liver and brain samples were collected to assess serum ammonia level, activities of alanine transaminase (ALT), and aspartate transaminase (AST), brain and liver oxidative stress parameters as well as histopathological investigations.TAA rats experienced increases in serum activities of ALT and AST as well as serum levels of ammonia. Furthermore, TAA induced hepatic and brain oxidative damage as indicated by increase in lipid peroxidation (LP), decrease in reduced glutathione (GSH) and decrease in superoxide dismutase (SOD) activity as well as increased nitric oxide (NO) levels. TAA caused distortion of hepatic and brain architecture as shown by histopathological examination. Treatment with α-LAC either alone or combined with vit. C resulted in improved liver functions by decline in serum AST and ALT activities and reduction in serum ammonia level. Alpha-LAC and vit. C reduced LP and NO levels while increased GSH concentration and SOD activity in hepatic and brain tissues. Finally, α-LAC-vit. C combination improved the hepatic and brain histological picture. Alpha-LAC-vit. C combination may be a promising pharmacological tool in providing a natural source of branched-chain amino acids and powerful antioxidants to combat hepatic encephalopathy-associated hyperammonemia and its consequential oxidative damage in liver and brain.

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“…ALT increases in serum when cellular degeneration or destruction occurs in this organ [33]. Any interference in these enzymes leads to biochemical impairment and lesions of the tissue and cellular function Yousef et al [35] reported that the changes in the activities of these enzymes in SnCl 2 -treated rats were regarded as the biochemical manifestation of the toxic action of inorganic tin. On the other hand, phosphatases and dehydrogenases are important and critical enzymes in biological processes too.…”

Section: Discussionmentioning

confidence: 99%

Effects of Subacute and Subchronic Treatment of Synthetic Plant Growth Regulators on Liver Damage Serum Biomarkers Tissue Antioxidant Defense Systems and Lipid Peroxidation in Rats

Özok¹,

Çelik²

2012

J Drug Metab Toxicol

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The present study was aimed to investigate the effects of some synthetic plant growth regulators; ß-Naphthoxy acetic acid (ß-NOA) and 4-Chlorophenoxy acetic acid (4-CPA) at 10 and 20 ppm dosages on liver damage, antioxidant defense system and lipid peroxidation in rats. Rats were divided into 12 groups as control, ß-NOA and 4-CPA at 10 and 20 ppm dosages application groups. Serum marker enzymes and biochemical parameters were selected as biomarkers for liver damage. Antioxidant defense systems as SOD, GR, CAT, GSH-Px, GST and G6PD enzyme activities and GSH and MDA contents were determined in tissues as the indicators of oxidative stress. At the end of experiments, the statistically significant changes were observed in the levels of TPRO, TALB, TCHOL, TBIL, AST, ALT and LDH as liver damage serum biomarkers in rats exposed to 10 and 20 ppm of ß-NOA and 4-CPA as compared with controls. MDA levels increased in all the tissues of rats exposed to ß-NOA and 4-CPA dosages whereas the fluctuation in SOD, GR, CAT, GSH-Px, GST and G6PD enzyme activities and GSH levels were observed compared with controls. It could be concluded that the treatments of ß-NOA and 4-CPA dosages may induce liver damage and oxidative stress.

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Study of the protective effect of ascorbic acid against the toxicity of stannous chloride on oxidative damage, antioxidant enzymes and biochemical parameters in rabbits

Cited by 44 publications

References 41 publications

Protective effect of ascorbic acid against oxidative damage induced by hydrogen peroxide in cultured human peripheral blood lymphocytes

Protective effect of ascorbic acid against oxidative damage induced by hydrogen peroxide in cultured human peripheral blood lymphocytes

Antioxidant and Hypo-Ammonemic Activities of Alpha-Lactalbumin and Vitamin C in Thioacetamide-Induced Liver and Brain Damage in Rats

Effects of Subacute and Subchronic Treatment of Synthetic Plant Growth Regulators on Liver Damage Serum Biomarkers Tissue Antioxidant Defense Systems and Lipid Peroxidation in Rats

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