|
|
Avicenna Journal of Medical Biochemistry، جلد ۲، شماره ۱، صفحات ۰-۰
|
|
|
| عنوان فارسی |
Hepatoprotective Effects of Vitamin E Against Malathion-Induced Mitochondrial Dysfunction in Rat Liver |
|
| چکیده فارسی مقاله |
Conclusions In conclusion, AT measurement can be beneficial for the safety or recovery of malathion-induced toxic injury in liver tissue and liver mitochondria. Results In liver tissue, the activity of LPO and CAT was higher in the malathion group in comparison to controls. AT reduced malathion-induced LPO, SOD, CAT, and GPx in rat liver. Coadministration of AT with malathion improved LPO, SOD, and CAT levels in liver as well as CAT and GPx in liver mitochondria. Malathion-induced mitochondria toxicity was recovered by AT. Materials and Methods The mitochondrial viability was determined in liver. Effective doses of malathion(200 mg/kg/day) and vitamin E (alpha-tocopherylacetate [AT]; 15 mg/kg/day) were administered alone or in combination for 14 days. At the end of the experiment, the liver tissue and liver mitochondria of the animals were harvested and examined. Objectives The aim of this study was to examine the protective function of vitamin E on toxicity of malathion, by measuring the activities of liver and liver mitochondrial superoxide dismutase (SOD), catalase (CAT),lipid peroxidation (LPO),and glutathione peroxidase (GPx) in rats. Background Malathion is an insecticide of the grouping of organophosphate pesticides (OPs), which shows strong insecticidal effects. In addition, vitamin E reacting to cell membrane site may prevent OP-induced oxidative injury. |
|
| کلیدواژه‌های فارسی مقاله |
|
|
| عنوان انگلیسی |
Hepatoprotective Effects of Vitamin E Against Malathion-Induced Mitochondrial Dysfunction in Rat Liver |
|
| چکیده انگلیسی مقاله |
Conclusions In conclusion, AT measurement can be beneficial for the safety or recovery of malathion-induced toxic injury in liver tissue and liver mitochondria. Results In liver tissue, the activity of LPO and CAT was higher in the malathion group in comparison to controls. AT reduced malathion-induced LPO, SOD, CAT, and GPx in rat liver. Coadministration of AT with malathion improved LPO, SOD, and CAT levels in liver as well as CAT and GPx in liver mitochondria. Malathion-induced mitochondria toxicity was recovered by AT. Materials and Methods The mitochondrial viability was determined in liver. Effective doses of malathion(200 mg/kg/day) and vitamin E (alpha-tocopherylacetate [AT]; 15 mg/kg/day) were administered alone or in combination for 14 days. At the end of the experiment, the liver tissue and liver mitochondria of the animals were harvested and examined. Objectives The aim of this study was to examine the protective function of vitamin E on toxicity of malathion, by measuring the activities of liver and liver mitochondrial superoxide dismutase (SOD), catalase (CAT),lipid peroxidation (LPO),and glutathione peroxidase (GPx) in rats. Background Malathion is an insecticide of the grouping of organophosphate pesticides (OPs), which shows strong insecticidal effects. In addition, vitamin E reacting to cell membrane site may prevent OP-induced oxidative injury. |
|
| کلیدواژه‌های انگلیسی مقاله |
|
|
| نویسندگان مقاله |
اکرم رنجبر | akram ranjbar
department of toxicology and pharmacology, hamadan university of medical sciences, hamadan, ir iran; department of toxicology and pharmacology, hamadan university of medical sciences, hamadan, ir iran. tel fax 98-8118380031
سازمان اصلی تایید شده: دانشگاه علوم پزشکی همدان (Hamadan university of medical sciences)
فریبا محسن زاده | fariba mohsenzadeh
department of biology, bu-ali sina university, hamedan, ir iran
سازمان اصلی تایید شده: دانشگاه بوعلی سینا (Bu ali sina university)
مریم بعیری | maryam baeeri
faculty of pharmacy, pharmaceutical sciences research center, tehran university of medical sciences, tehran, ir iran
سازمان اصلی تایید شده: دانشگاه علوم پزشکی تهران (Tehran university of medical sciences)
|
|
| نشانی اینترنتی |
http://www.avicennajb.com/index.php?page=article&article_id=18321 |
| فایل مقاله |
فایلی برای مقاله ذخیره نشده است |
| کد مقاله (doi) |
10.17795/ajmb-18321 |
| زبان مقاله منتشر شده |
fa |
| موضوعات مقاله منتشر شده |
|
| نوع مقاله منتشر شده |
research-article |
|
|
|
برگشت به:
صفحه اول پایگاه |
نسخه مرتبط |
نشریه مرتبط |
فهرست نشریات
|