Histological and ultrastructural study of AflatoxinB1 induced neurotoxicity in Sciatic nerve of adult male Albino rats.

Aflatoxins are mycotoxins produced by Aspergillus spp. which is a common contaminant of food items such as corn, spices, rice, nuts, and flour. Aflatoxin contamination of foods is a worldwide problem. Chronic aflatoxin exposure is found to be associated with Sciatic nerve damage. In vivo study was carried out to evaluate the toxic effect of aflatoxin B1 (AFB1) on the Sciatic nerve. Twenty-one adult male rats were included and divided equally into 3 groups (7 rats each): Group I (control group), group II (olive oil group) and group III: (AflatoxinB1 group). The rats received AFB1 (250 µg/kg B.W./day) orally by gastric tube 5 days/week for 4 weeks. Sciatic nerve specimens were prepared, and semi-thin sections were stained with Toluidine blue, examined by light microscope and photographed. Ultrathin sections (50-80 nm) from selected areas of the trimmed blocks were made, examined and photographed by transmission electron microscopy (JEOL-JSM-1011) in King Saud University Electron Microscopy Unit. The findings indicate that the administration of AFB1 to rats' results in degeneration in the sciatic nerve in the form of Wallerian degeneration in the myelin sheath. Macrophages appear to engulf the degenerated myelin and neutrophils.

Modulation of oxidative stress by Chlorella vulgaris in streptozotocin (STZ) induced diabetic Sprague-Dawley rats.

PURPOSE: Chlorella vulgaris (CV), a fresh water alga has been reported to have hypoglycemic effects. However, antioxidant and anti-inflammatory effects of CV in diabetic animals have not been investigated to date. The aim of the present study was to investigate the role of CV in inflammation and oxidative damage in STZ-induced diabetic rats. MATERIALS AND METHODS: Male Sprague-Dawley rats (300 - 400g) were divided into 4 groups: control, CV, STZ-induced diabetic rats, and STZ rats treated with CV (150mg/kg body wt). Blood samples were drawn from orbital sinus at 1 and 4 weeks for determination of oxidative cellular damage (DNA damage and lipid peroxidation [malondialdehyde, MDA]), inflammation (tumour necrosis factor alpha, TNF-α) and antioxidant status (catalase, CAT, and superoxide dismutase, SOD). RESULTS: CV did not have any effects on glucose levels in diabetic rats, over the 4 weeks of treatment. However, it reduced significantly DNA damage and blood MDA levels in STZ-induced diabetic rats compared to the control group. Plasma levels of TNF-α however did not show any significant changes in STZ-induced diabetic rats fed with CV. Antioxidant enzyme SOD showed no significant changes in all groups but CAT activity was reduced in STZ-induced diabetic rats compared to the control. CONCLUSIONS: CV did not have hypoglycaemic effect but it has a protective role in STZ-induced diabetic rats by reducing oxidative DNA damage, and lipid peroxidation.