Abstract:Methanol, a highly toxic substance, is used as an industrial solvent and in automobile antifreeze. Acute methanol poisoning produces severe metabolic acidosis and serious neurologic sequelae. We describe a 50-year-old woman with accidental methanol intoxication who was in a vegetative state. MRI showed haemorrhagic necrosis of the putamina and oedema in the deep white matter.
“…8 The bilateral haemorrhagic necrosis of the putamen and oedema in the deep white matter of our patient are the characteristic MRI findings of severe methanol intoxication. 9 Besides the optic disc oedema, the oedematous changes involving optic tracts and optic radiations shown on MRI might contribute to the profound vision loss in our case. The MRI in methanol poisoning not only demonstrates this specific pattern of brain damage but also provides good correlation among brain, visual pathway, and the evolution of the clinical course of the disorder.…”
“…8 The bilateral haemorrhagic necrosis of the putamen and oedema in the deep white matter of our patient are the characteristic MRI findings of severe methanol intoxication. 9 Besides the optic disc oedema, the oedematous changes involving optic tracts and optic radiations shown on MRI might contribute to the profound vision loss in our case. The MRI in methanol poisoning not only demonstrates this specific pattern of brain damage but also provides good correlation among brain, visual pathway, and the evolution of the clinical course of the disorder.…”
“…Accidental or suicidal ingestion can cause severe metabolic acidosis and clinical disturbances such as blindness, serious neurologic sequelae and death (Kuteifan et al, 1998;Liu et al, 1998). Methanol is being increasingly recognized as a substance that damages the liver cells where it is oxidized to formaldehyde and latter to formate (Trocho et al, 1998).…”
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.
“…A relatively small amount of aspartame can significantly increase plasma methanol levels 2) . Accidental or suicidal ingestion can cause severe metabolic acidosis and clinical disturbances such as blindness, serious neurologic sequelae and death 3,4) . Methanol is being increasingly recognized as a substance that damages the liver cells where it is oxidized to formaldehyde and later to formate 5) .…”
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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