Abstract
Lead is a common industrial poison that persists in the environment and has many toxic effects on different organs & tissues especially on the central nervous system. This study aimed to investigate the effects of lead administration on cerebellar cortex of adult male albino rats and the possible protecting effects of vitamin E. Materials and Methods: Forty male albino rats, (160 ± 10 g weight) were divided into four groups, ten rats each. In the control group rats were received distilled water daily, 2nd group rats were given 30 mg/ kg lead acetate dissolved in distilled water orally daily for two months, 3rd group rats were pretreated by 100 mg/ kg vit. E orally 6 hours before administration of lead acetate by the same dose as group 2 for two months, the 4th group rats were given the same dose of lead acetate then withdrawal was done for one month. Tissue specimens then prepared for light and electron microscopic examinations. The results: By light microscope, in rats treated with lead, the number of Purkinje cells showed a significant decrease in comparison to control group, and appeared shrunken, distorted in shape with irregular nuclei, while in rats treated with lead and vitamin E, there was marked improvement of these alterations. Electron microscopic examination showed Purkinje cells with ill defined nucleus, vaculated or rarified cytoplasm and small electron dense mitochondria. Granular cells showed vaculated cytoplasm and mitochondria with destroyed cristae. In case of vitamin E administration, marked protection against these changes was observed, while the withdrawal group showed very little or no improvement.
Highlights
This study aimed to investigate the effects of lead administration on cerebellar cortex of adult male albino rats and the possible protecting effects of vitamin E
In the control group rats were received distilled water daily, 2nd group rats were given 30 mg/ kg lead acetate dissolved in distilled water orally daily for two months, 3rd group rats were pretreated by 100 mg/ kg vit
E orally 6 hours before administration of lead acetate by the same dose as group 2 for two months, the 4th group rats were given the same dose of lead acetate withdrawal was done for one month
Summary
Lead (Pb) is a highly toxic heavy metal that persists in the environment and the human body and can disrupt neurological & other biological body functions ( Bauchi et al, 2016).chronic poisoning by it is one of the major public health hazards especially in developing countries (Flora et al, 2012).Small amount of lead is excreted in urine and the rest accumulates in various body tissues, mainly the (CNS) which may result in structural changes that can persist even after lowering of its blood level (Sidhu and Nehru, 2004; Taib et al, 2004; Flora et al, 2006; Ibrahim et al, 2012).Lead was reported to produce oxidative stress by generating release of reactive oxygen species (ROS) such as superoxide radicals, hydroxyl radicals, hydrogen peroxide and lipid peroxides which increase oxidative damage of cellular materials (Ercal et al, 2001 and El-Nekeety et al, 2009).Depending on the observation that free radicals were generated during the pathogenesis processes induced by lead, it was presumed that supplementation of antioxidants will interrupt or minimize the damaging effects of lead and improve the effects of chelating agents (Flora et al, 2003).Vitamin E is a lipid soluble membrane-bound antioxidant which protects cell membrane against oxidative stress (Soylu et al, 2006), and has powerful neuro-protective effects (Crouzin et al 2010). Lead (Pb) is a highly toxic heavy metal that persists in the environment and the human body and can disrupt neurological & other biological body functions ( Bauchi et al, 2016).chronic poisoning by it is one of the major public health hazards especially in developing countries (Flora et al, 2012). Lead was reported to produce oxidative stress by generating release of reactive oxygen species (ROS) such as superoxide radicals, hydroxyl radicals, hydrogen peroxide and lipid peroxides which increase oxidative damage of cellular materials (Ercal et al, 2001 and El-Nekeety et al, 2009). Vitamin E is a lipid soluble membrane-bound antioxidant which protects cell membrane against oxidative stress (Soylu et al, 2006), and has powerful neuro-protective effects (Crouzin et al 2010).
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