التفاصيل البيبلوغرافية
| العنوان: |
Chronic neurodegeneration by aflatoxin B1 depends on alterations of brain enzyme activity and immunoexpression of astrocyte in male rats. |
| المؤلفون: |
Alsayyah, Ahmed, ElMazoudy, Reda, Al-Namshan, Mashael, Al-Jafary, Meneerah, Alaqeel, Nouf |
| المصدر: |
Ecotoxicology & Environmental Safety; Oct2019, Vol. 182, pN.PAG-N.PAG, 1p |
| مصطلحات موضوعية: |
GLUTATHIONE peroxidase, GLIAL fibrillary acidic protein, ACID phosphatase, ENZYMES, NEURODEGENERATION, LACTATE dehydrogenase |
| مستخلص: |
Aflatoxin B1 poses the greatest risk among the mycotoxins to target-organisms particularly human, however, no studies addressed the neurotoxicity of chronic exposure of aflatoxin. The oral dose level 1/600th of LD50 for 30, 60, and 90 days was used for three aflatoxin groups, respective to negative and vehicle control groups. Activity levels of brain antioxidants viz: superoxide dismutase, catalase, glutathione, and glutathione peroxidase significantly decreased in the three experimental durations in time-dependent trend, in contrast, lipid peroxidation showed a significant increase compared to controls. Significantly, chronic-dependent increase trend was noticed in the AF60 and AF90 group for acid phosphatase (16.1%, 35.2%), alkaline phosphatase (32.1%, 50.8%), aspartate aminotransferase (38.7%, 120.0%) and lactate dehydrogenase (30.6%, 42.1%) activities, respectively. However, a significant 23.7% decrease in the brain creatine kinase activity following 90 days of AFB1administration. Chronic administration of aflatoxin also causes alterations in activities of protein carbonyl with a maximum increase (twofold) after 90 days. Further, histopathological and immunohistochemical results confirmed time-related vasodilation, necrosis and astrocytes gliosis by high glial fibrillary acidic protein immunostaining in response to AFB1. These findings infer that long-term exposure to AFB1 results in several pathophysiological circumstances in a duration-dependent manner concerning neurodegeneration especially Alzheimer's disease. • Oxidative activities of chronic aflatoxin B1 exposure to male rat brain and the astrocytes gliosis by GFAP immunohistochemistry were assessed. • Aflatoxin B1 increased brain enzyme activities and malondialdehyde levels in the brain of rats in a time-trend manner. • The time accumulation elevated astrocytes clumping and deteriorated neuronal histology. • The data will aid future studies of the mechanism of the neurodegeneration. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
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