ABSTRACT
Aluminium has the potential to be neurotoxic in human and animals and excess aluminium exposure has been implicated in the pathogenesis of several clinical disorders as dialysis encephalopathy and Alzheimer disease. The present study was carried out to determine the effectiveness of ginkgo biloba leaf extract [GBE] in alleviating the neurotoxicity of aluminium chloride [A1C13] in adult male albino rats. Seventy five adult male albino rats were divided into 4 groups: Control groups [a, negative control b, distilled water] Alcl3 group [200mg/kg/orally/daily] Ginkgo group [100 mg/kg /orally/daily] and Alcl3 + Ginkgo group [A1C13 200mg/kg + Ginkgo 100 rng/kg /orally/daily]. After 8 weeks of treatment, rats were sacrificed and brain were dissected out and subjected to estimation of activity of antioxidant enzymes [glutathione peroxidase [GPX], superoxide disrnutase [SOD], catalase [CAT]], histological and immunohistochemical staining of beta-amyloid proteins. The result of this study revealed that AlcB induced a significant reduction in antioxidant enzymes activity with neurofibrillary tangles and nuclear deformity in neurol cells with increased aggregation of beta amyloid proteins. Concomitant administration of Ginkgo biloba leaf extract with AlcB resulted in a significant increase in antioxidant enzymes activity and alleviation of histopathological changes induced by aluminium. Also a marked reduction in expression of beta amyloid proteins was observed. It was concluded that GBE has a protected effect against aluminium chloride induced neurotoxicity and this protection could be attributed to its antioxidant activity and its ability to suppress amyloid proteins aggregation in brain tissue?
ABSTRACT
Cypermethrin is a synthetic pyrethroid with a potent insecticidal property. Both agricultural and residential usage is continuing to grow leading to increased human exposure to this compound. Cypermethrin has been found to has neurotoxic, mutagenic, carcinogenic effects and it also has been found to have estrogen like effect. The present study was carried out to predict the effect of cypermethrin on male albino rats fertility. Thirty sexually mature male albino rats were used and classified into 3 equal groups. Group I: negative control, Group II: received orally daily 2ml corn oil, Group III received orally daily 25mg/kg body weight of cypermethrin dissolved in 2ml corn oil. The study was extended for 65 days. At the end of the study the rats were weighed then, blood were obtained for testosterone level estimation and the rats were sacrificed. The testis and epididyms were excised. Epididymal spermatozoa were examined and the testis were prepared for histopathological examination. The results of the present study revealed that Cypermethrin induced a significant decreases in animals body weight gain, testicular weight, serum testosterone, epididymal spermatozoal concentration and the percentage of live and motile sperms, while sperm head and tail abnormalities were significantly, increased. Histopathological examination of the testis revealed thinning of the wall of seminiferous tubules, interstitial tissues showed cellular infiltration, congested blood vessels, edema fluid and connective tissues. It was concluded that cypermethrin induced adverse effects on male fertility parameters in mature male albino rats
ABSTRACT
Methanol toxicity produces toxic injuries to the retina and optic nerve results in blindness. Formic acid [the toxic metabolite responsible for these toxic effects] is a mitochondrial toxin that increases the production of Reactive Oxygen Species resulting in oxidative stress cell injury. In the retina, glutathione acts as a vital defense mechanism against oxidative stress. N-acetylcysteine [NAC] is a glutathione precursor and acts as a free radical scavenger. In this study the role of NAC against methanol-induced retinal toxicity was evaluated in adult male albino rats. Group [I] [control: received normal saline], group [IIa]: [received daily oral toxic dose of methanol 3gmlkg for 72 hrs], group [IIb] [follow up group]: [received daily oral toxic dose of methanol 3gmlkg for 72 hrs then saved for follow up for 24 hrs], group [IIc]: [received daily oral toxic dose of methanol 3gm/kg for 72 hrs and single oral therapeutic dose of NAC 800mg/kg 24 hrs after the last dose of methanol], group [III]: [received single oral therapeutic dose of NAC 800mg/kg]. After the period of each group, the rats were sacrificed and were investigated by assessment of glutathione, glutathione peroxidase activity, histopathological and ultrastructural examination of retinal tissue. Methanol-toxicity induced a significant decrease in glutathione and glutathione peroxidase activity, with retinal edema and vaculation of photoreceptors inner segment and enlarged irregularly stained nuclei, and profound mitochondrial swelling with severely disrupted cristae, as compared with control. Follow up group showed a significant decrease in glutathione and glutathione peroxidase, as compared with control, and a significant increase in its activity as compared with methanol-toxicity, with mild alterations in photoreceptor mitochondria. NAC-treated group revealed a significant increase in glutathione and glutathione peroxidase, as compared with methanol toxicity, and a non significant difference in comparison with control and NAC groups, with normal retinal structures. It is concluded that methanol induced severe retinal toxicity that could be reversed by N-acetylcysteine administration through its action as a glutathione precursor and a free radical scavenger