23-08-2013, 04:13 PM
Role of Se+Zn in Regeneration (Ki67) Following Pb Toxicity in Wistar rat.
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Introduction
Lead poisoning is a serious health [reblem in the developing countries, (WHO 2002)
Causes reproductive toxicity via the suppression of spermatogenesis and Androgenesis in males Apostoli and Catalini 2011), (Benoff et al., 2000; Akinloye et al 2006 ), Fukushima et al., (2005), Yi Lu ( 2009), Salgado et al (2010).
Overall aim
The aim of this study is to determine the effect of selenium and zinc on lead-induced testicular damage in Sprague-Dawley Rats.
The Specific objectives
The specific objective of this study are to determine the effect of
Selenium and zinc supplementation on the activities of Ki 67 (a proliferation marker) following treatment with lead
Selenium and zinc on the activities of P53 and CaD in lead induce-testicular damage
Immunohistochemistry
Paraffin wax embedded sections were mounted on a glass slide in preparation for antigen retrieval.
Immersed in Urea overnight and placed in microwave for 45 mins
Primary and secondary antibodies application
( Biotinylated goat serum for 1hr. And 1% Bovine serum albumin)
Discussion
The cytoplasmic pathway was observed to be the most predominant in lead toxicity, although oxidative stress is primary, it is important to distinguish the resultant forms of cell death in the germinal epithelium
Apoptotic pathway was predominant as seen in the lead treated group 2( Fig 1b,2b,3b, and 4b), although necrosis was observed in the sertoli cells closer to the BM
Summary and Conclusion
Pb toxicity can follow a mitochondria pathway (CAD) or a cytoplasmic pathway involving P53, the most predominant form of cell death is apoptosis which can result from both pathways.
Se+Zn treatment improves proliferation and counters Pb toxicity by substitution, activation of enzymes and Growth factors, Endothelial factors, and radical scavengers.