Effect of Methanol or Modifications of the Hepatic Glutathione Concentration on the Metabolism of Dichloromethane to Carbon Monoxide in Rats

Pankow, D; Jagielki, S.

doi:10.1177/096032719301200305

Cited by 31 publications

(13 citation statements)

References 23 publications

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“…Depletion of GSH increases vulnerability to free radical induced damage. The decrease in GSH concentration observed in the present study seems to have been caused by methanol intoxication because methanol metabolism depends upon GSH 43) . In addition, a decrease in GSH concentration would also be caused by its rapid reaction with the highly reactive compound, formaldehyde, which is generated during methanol metabolism, forming nucleophilic adducts and/or LPO products 44,45) .…”

Section: Discussionmentioning

confidence: 48%

Methanol‐Induced Oxidative Stress in Rat Lymphoid Organs

Parthasarathy

Kumar

Manikandan

et al. 2006

Journal of Occupational Health

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Methanol-Induced Oxidative Stress in Rat Ly m p h o i d O r g a n s : N a r a y a n a p e r u m a l J . PARTHASARATHY, et al. Immunology Laboratory, Department of Physiology, Dr. ALM. PG. Institute of Basic Medical Sciences, University of Madras, Taramani Campus, India-Methanol is primarily metabolized by oxidation to formaldehyde and then to formate. These processes are accompanied by formation of superoxide anion and hydrogen peroxide. This paper reports data on the effect of methanol on antioxidant status and lipid peroxidation in lymphoid organs such as the spleen, thymus, lymph nodes and bone marrow of rats. Male Wistar albino rats were i n t o x i c a t e d w i t h m e t h a n o l ( 2 . 3 7 g / k g b . w intraperitoneally) for detecting toxicity levels for one day, 15 d and 30 d, respectively. Administration of methanol at 15 and 30 d significantly (p<0.05) increased lipid peroxidation and decreased the enzymatic (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymatic antioxidants (reduced glutathione and vitamin C) in lymphoid organs. However, lipid peroxidation and enzymatic and nonenzymatic antioxidants in the acute methanol exposed group animals were found to be significantly (p<0.05) increased. In one day methanol intoxication, the levels of free radicals initially increased, and to remove these free radicals, antioxidants levels were elevated, which generally prevented oxidative cell damage. But in longer periods of intoxication, when the generation of reactive free radicals overwhelmed the antioxidant defense, lipid peroxidation increased. Further, decreased antioxidants in 15 and 30 d methanol intoxication may have been due to overutilization of non-enzymatic and enzymatic antioxidants to scavenge the products of lipid peroxidation. In addition, the liver a n d k i d n e y m a r k e r s o f s e r u m a s p a r t a t e aminotransferase (AST), alanine aminotransferase (ALT), urea and creatinine significantly increased. This study concludes that exposure to methanol causes oxidative stress by altering the oxidant/antioxidant balance in lymphoid organs of the rat. (J Occup Health 2006; 48: 20-27)

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Section: Discussionmentioning

confidence: 48%

Methanol‐Induced Oxidative Stress in Rat Lymphoid Organs

Parthasarathy

Kumar

Manikandan

et al. 2006

Journal of Occupational Health

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“…So the decrease in cellular glutathione content increases cell vulnerability to oxidative stress (Meister and Anderson, 1983;Oyama et al, 2002). The decrease in GSH activity observed in the present study seems to have been caused by methanol, because methanol metabolism depends upon GSH (Pankow and Jagielki, 1993). In addition, a decrease in GSH content would also be caused by its rapid reaction with the highly reactive compound, formaldehyde, which is generated during methanol metabolism forming nucleophilic adducts and/ or LPO products (Shrzylewska and Farbisewski, 1996;Parthasarathy et al,2006).…”

Section: Discussionmentioning

confidence: 58%

Effect of aspartame on some oxidative stress parameters in liver and kidney of rats

Iman¹

2011

Afr. J. Pharm. Pharmacol.

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Aspartame is one of the most widely used artificial sweeteners in over 90 countries worldwide. It is a highly intensity sweetener added to a large variety of food, most commonly found in low calorie beverages, desserts and table top sweeteners added to tea or coffee. The present study examined whether the daily oral administration of ASP (40 mg/kg) for 2, 4 and 6 weeks induce oxidative stress in the liver and kidney of male albino rats. Lipid peroxidation (LPO), glutathione reduced (GSH) levels as well as the activities of superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT) enzymes were determined. A significant increase in LPO levels was obtained in the liver tissue after 4 and 6 weeks of ASP administration while there was a significant decrease in LPO level after 2 weeks followed by a significant increase in the renal tissue at the end of the 6 weeks. SOD activity significantly decreased in the liver tissue after 2, 4 and 6 weeks of treatment. Also, there was a significant decrease in SOD activity after 2 and 4 weeks in the renal tissue. CAT activity significantly decreased in the liver tissue after 2 and 4 weeks of ASP administration. Regarding to GSH content, there was a significant decrease in the liver tissue after 2, 4 and 6 weeks which was accompanied by a significant increase in GST activity after 4 and 6 weeks of ASP administration. In conclusion, ASP may induce an oxidative stress in the liver and kidney of male albino rats.

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“…Though during 15 days of aspartame administration it could elevate GSH level, but after 30 and 90 days of administration the drastic decrease in GSH may be a contributing factor for the nitric oxide level increase. The decrease in GSH activity observed in the present study could be caused by methanol, because methanol metabolism depends upon GSH (Pankow and Jagielki, 1993). The decrease in cellular glutathione content increases cell vulnerability to oxidative stress (Oyama et al, 2002).…”

Section: Discussionmentioning

confidence: 55%

Imbalance of the oxidant - antioxidant status by aspartame in the organs of immune system of Wistar albino rats

Choudhary¹,

Devi²

2014

Afr. J. Pharm. Pharmacol.

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Aspartame (L-aspartyl-L-phenylalanine methyl ester) is one of the most widely artificial sweeteners consumed in so many products worldwide in various countries which added to a large variety of food, most commonly found in low calorie beverages. On metabolism in humans and experimental animals, aspartame is rapidly and completely metabolized to aspartic acid (40%), phenylalanine (50%) and methanol (10%). Methanol, a toxic metabolite is primarily metabolized by oxidation to formaldehyde and then to formate; these processes are accompanied by the formation of superoxide anion and hydrogen peroxide. This study focus is to understand whether the oral administration of aspartame (40 mg/kg b.w) for 15, 30 and 90 days have any effect on the antioxidant status (enzymatic and non-enzymatic) in immune organs such as the spleen, thymus, lymph nodes and bone marrow of rats. To mimic human methanol metabolism, folate deficient rats were used. After 15 days of aspartame administration, animals showed a significant increase in free radical production as indicated by the increase in both enzymatic (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymatic (reduced glutathione and vitamin C) antioxidant level along with the marked increase in lipid peroxidation and nitric oxide level. However, after repeated long term administration (30 and 90 days), the generation of reactive free radicals overwhelmed the antioxidant defense as indicated by an increase in lipid peroxidation with the decrease in antioxidants level. This study concludes that administration of aspartame even at the Food and Drug Administration permitted level its repeated exposure causes oxidative stress by altering the oxidant/antioxidant balance in immune organs of the rats and its effects also reflected in the histology of the spleen and lymph nodes

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Effect of Methanol or Modifications of the Hepatic Glutathione Concentration on the Metabolism of Dichloromethane to Carbon Monoxide in Rats

Cited by 31 publications

References 23 publications

Methanol‐Induced Oxidative Stress in Rat Lymphoid Organs

Methanol‐Induced Oxidative Stress in Rat Lymphoid Organs

Effect of aspartame on some oxidative stress parameters in liver and kidney of rats

Imbalance of the oxidant - antioxidant status by aspartame in the organs of immune system of Wistar albino rats

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