Influences of Different Stress Models on the Antioxidant Status and Lipid Peroxidation in Rat Erythrocytes

Abstract Gallic acid has been identified as an antioxidant component of the edible and medicinal plant Peltiphyllum peltatum. The present study examined its potential protective role against sodium fluoride (NaF)-induced oxidative stress in rat erythrocytes. Oxidative stress was induced by NaF administration through drinking water (1030.675 mg m-3 for one week). Gallic acid at 10 mg kg-1 and 20 mg kg-1 and vitamin C for positive controls (10 mg kg-1) were administered daily intraperitoneally for one week prior to NaF administration. Thiobarbituric acid reactive substances, antioxidant enzyme activities (superoxide dismutase and catalase), and the level of reduced glutathione were evaluated in rat erythrocytes. Lipid peroxidation in NaF-exposed rats significantly increased (by 88.8 %) when compared to the control group (p<0.05). Pre-treatment with gallic acid suppressed lipid peroxidation in erythrocytes in a dose-dependent manner. Catalase and superoxide dismutase enzyme activities and glutathione levels were reduced by NaF intoxication by 54.4 %, 63.69 %, and 42 % (p<0.001; vs. untreated control group), respectively. Pre-treatment with gallic acid or vitamin C significantly attenuated the deleterious effects. Gallic acid isolated from Peltiphyllum peltatum and vitamin C mitigated the NaF-induced oxidative stress in rat erythrocytes.

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Antioxidant status and lipid peroxidation in hereditary haemochromatosis Young IS, Trouton TG, Torney JJ, McMaster D, Callender ME, Trimble ER. Free Rad Biol Med 1994;16:393?397

Hepatology ◽

10.1016/0270-9139(95)90274-0 ◽

1995 ◽

Vol 21 (4) ◽

pp. 1195

Keyword(s):

Lipid Peroxidation ◽

Antioxidant Status ◽

Hereditary Haemochromatosis

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The Impact of Concomitant Chronic Pancreatitis on Prooxidant-antioxidant Status and Other Conditions in Osteoarthritis

Family Medicine ◽

10.30841/2307-5112.6.2016.249507 ◽

2016 ◽

pp. 75-78

Author(s):

Liliia Babynets ◽

Tetiana Maevska

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Superoxide Dismutase ◽

Chronic Pancreatitis ◽

Functional Capacity ◽

Antioxidant Status ◽

Activation Parameters ◽

Tissue Destruction ◽

The Impact ◽

Stress Accumulation

The study proved that patients with combined progress of osteoarthritis and chronic pancreatitis have reliable top-level activation of lipid peroxidation in terms of malonyc aldehyde and tissue destruction in terms of oxyproline, weakening of the antioxidant level (in terms of superoxide dismutase and SH-groups) and activation parameters of catalase and ceruloplasmin (p<0,05). The authentic predictority of patients biological age, duration of combined clinical courses, the functional capacity of the pancreas in terms of fecal α-elastase, structural state by ultrasound criteria for progression effects of oxidative stress, accumulation oxyproline activation parameters catalase and ceruloplasmin, which statistically was reflected by the presence of mainly moderate of significant correlations between these groups of indicators have been identified.

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Lipid peroxidation parameters and antioxidant status of critically ill intensive care unit patients

Critical Care ◽

10.1186/cc142 ◽

1998 ◽

Vol 2 (Suppl 1) ◽

pp. P012 ◽

Cited By ~ 2

Author(s):

KH Smolle ◽

G Khoschsorur ◽

W Wonisch ◽

F Tatzber

Keyword(s):

Intensive Care Unit ◽

Lipid Peroxidation ◽

Intensive Care ◽

Critically Ill ◽

Antioxidant Status

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Influence of cadmium ions on the antioxidant status and lipid peroxidation in mouse liver: protective effects of zinc and selenite ions

Trace Elements and Electrolytes ◽

10.5414/te0x1229 ◽

2012 ◽

Vol 29 (04) ◽

pp. 137-142 ◽

Cited By ~ 2

Author(s):

Rasa Bernotiene ◽

Laima Ivanoviene ◽

Ilona Sadauskiene ◽

Arunas Liekis ◽

Leonid Ivanov

Keyword(s):

Lipid Peroxidation ◽

Mouse Liver ◽

Antioxidant Status ◽

Protective Effects ◽

Cadmium Ions

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Multivitamin and mineral supplementation in 1,2-dimethylhydrazine induced experimental colon carcinogenesis and evaluation of free radical status, antioxidant potential, and incidence of ACF

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y11-100 ◽

2012 ◽

Vol 90 (1) ◽

pp. 45-54 ◽

Cited By ~ 1

Author(s):

Albert Baskar Arul ◽

Ignacimuthu Savarimuthu ◽

Mohammed A. Alsaif ◽

Khalid S. Al Numair

Keyword(s):

Lipid Peroxidation ◽

Antioxidant Status ◽

Reduced Glutathione ◽

Colon Carcinogenesis ◽

Aberrant Crypt Foci ◽

Lipid Hydroperoxides ◽

Entire Study ◽

Lipid Peroxidation Products ◽

Histopathological Alterations ◽

Mineral Supplementation

This study was performed to determine the chemopreventive and antioxidant status of multivitamin and mineral (0.01% in drinking water, ad libitum) supplements in 1,2-dimethylhydrazine (DMH)-induced experimental colon carcinogenesis. Experimental colon carcinogenesis was induced in male albino Wistar rats by injecting DMH (20 mg·(kg body mass)–1) once weekly for 15 consecutive weeks, and administering a multivitamin supplement in 3 regimes (initiation, post-initiation, and entire experimental period) for 32 weeks. We studied lipid peroxidation products (thiobarbituric acid reactive substances, lipid hydroperoxides, conjugated dienes) in the circulation and in the tissues, antioxidant status (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and non-enzymatic antioxidant-reduced glutathione) of the tissues, aberrant crypt foci (ACF), and histopathological alterations. DMH-induced rats had an increase in lipid peroxidation products and a lower antioxidant status compared with control animals. Multivitamin and mineral supplementation during the initiation, post-initiation, and the entire study period significantly decreased the levels of lipid peroxidation products in circulation and colonic tissues, significantly elevated the activities of the antioxidant enzymes and reduced glutathione to near normalcy in DMH-induced rats. The incidence of ACF was reduced to 84.1% in rats supplemented with multivitamin and minerals for the entire study and prevented the colonic tissue from histopathological alterations induced by DMH.

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