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Articles by A.S.A. Haffor
Total Records ( 2 ) for A.S.A. Haffor
  I.M. Alhazza and A.S.A. Haffor
  Heavy metal toxicity causes impairment of variety of cellular process. Cellular failure to maintain balance between the generation and elimination of reactive molecules results in tissue damage. The purpose of this study was to determine the effects of Lead (BP) toxicity on Free Radicals (FR) production. Sixteen adult rats matched with age were randomly assigned to two groups, control and experimental. The experimental group was injected (IP) 1 mg kg-1 of body weight BP daily for seven days. Mean FR in the control group was 206.13±12.39 CARR U. In BP treated group the mean (±SEM) FR rose to 324.13±12.61 CARR U. The change in FR corresponds to 57% increase in the lead treated group. Thus, BP toxicity exposure mediates mitochondria damage and the subsequent oxidative stress. Based on the results of the present study, it can be concluded that BP toxicity causes elevation of Reactive Oxygen Species (ROS) which mediate inhibition of mitochondrial respiration in rats.
  A.S.A. Haffor and I.M. Alhazza
  The purpose of the present study was to examine the separate and the combined effects of lead and hyperoxia in adult rats, Ratus ratus on LDH. Thirty-two rats were assigned randomly to control (C) and three experimental groups: lead (BP), hyperoxia (HP) and Hypaeroxia-Lead (HPBP). The mean (±SEM) activity of LDH rose significantly (p<0.05) from 216.41±12.39 U L-1 in control group to 539.28±28, 512.78±16.09 and 465.94±55.88 in BP, HP and HPBP groups, respectively. Therefore, both the separate and the combined effects of heavy metal lead and hyperoxai involve activation of LDH to compensate for cellular changes in the cytoplasm. Based on the results of the present study, it can be concluded that lead induces similar effects to hyperoxia exposure that causes the formation of Reactive Oxygen Species (ROS) which mediate changes in the cytoplasm enzymes such as LDH in rats.
 
 
 
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