University of Khartoum

Effect of Testosterone and Heat Stress on Muscles Protein Metabolism and Resistance to Plasmodium berghei Infection in Mice

Effect of Testosterone and Heat Stress on Muscles Protein Metabolism and Resistance to Plasmodium berghei Infection in Mice

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Title: Effect of Testosterone and Heat Stress on Muscles Protein Metabolism and Resistance to Plasmodium berghei Infection in Mice
Author: Mohammed, Muawia Abdalla Abdagalil
Abstract: The study was conducted in the Department of Biochemistry, Faculty of Veterinary Medicine, University of Khartoum, to determine the effect of Plasmodium berghei-ANKA malaria infection on muscle protein metabolism and resistance under different levels of the testosterone hormone and heat stress in Swiss albino male mice. Three experiments were conducted. In the first experiment, 60 male mice kept at room temperature (24±1°C) were divided into 6 groups (10 mice/group): two of normal testosterone level(control), two of high testosterone level and two of low testosterone level (castrated groups). One of each testosterone level was inoculated with 1 × 106 P.berghei -infected erythrocytes. Parasitemia and body weight were evaluated during the experimental periods(60 days). All mice were sacrificed after the experiment and blood was collected to investigate total protein, albumin, total globulin, creatinine, urea, alanine aminotransferase (ALT), aspartate aminotransferase (AST), cortisol and testosterone. Extensor digitorum longus (EDL) muscle was dissected with intact tendons and processed for tyrosine release assay. In this experiment, parasitemia was found to be significantly higher in the high testosterone level group than in the infected control group of normal testosterone level, whereas such difference was not found in the castrated infected group. Also, the high testosterone level in the infected mice caused significant decrease in total protein, albumin, total globulin and urea, and significant increase in AST, ALT and cortisol compared to the control group. No significant differences in muscle tyrosine release were obtained between the high testosterone infected group and control group. Castrated infected mice showed a significant increase in total globulin, AST and cortisol, accompanied by significant increase in muscle tyrosine release and significant decrease in body weight gain than in the control group. In addition, castrated groups showed significant reduction of body weight gain compared to the control group. In the second experiment similar groups were used and were exposed to heat stress (41±1°C). When mice subjected to heat stress, parasitemia was found to be significantly higher in the high testosterone group than the infected control group. The high testosterone level in the infected mice caused significant decrease in total protein, albumin, total globulin and AST activities, accompanied by significant elevation in creatinine, urea, and muscle tyrosine release compared to control group. Castrated infected mice showed a significant increase in creatinine, urea, cortisol and muscle tyrosine release, and significant decrease in AST activities compared to the control group. Also, significant decrease in body weight gain was recorded in all groups of mice subjected to heat stress compared to the control group. In the third experiment, eight groups of experimental mice (10 mice/group) were used. Three groups were inoculated with 1 × 106 P.berghei infected erythrocytes and one non-infected group was kept at room temperature. The infected groups consisted of normal testosterone level, high testosterone level and castrated group as low testosterone level, and non-infected group with normal testosterone level (control group). The other four groups treated similar to the previous ones, were exposed to heat stress. All animals in this experiment were not sacrificed and monitored for differences in survival rate, to evaluate the effect of heat stress and infection on the animals life span. In the third experiment, high testosterone level caused a significant decrease in survival rate in infected mice kept at room temperature or subjected to heat stress. The present findings suggest that testosterone level is key mediator in response to P.berghei infection in male mice and produced significant effects in certain blood biochemical values, parasitemia and body weight. Moreover, castration reversed the adverse effects caused by high testosterone levels. Also testosterone level played a significant role in altering muscle protein metabolism during malaria and influenced the effect of heat stress. However, infected animals of high testosterone levels showed similar survival rate, when subjected to heat stress or kept at room temperature. On the other hand, the infected castrated and normal testosterone level groups were negatively influenced by the heat stress, and they showed shorter life span than similar ones kept at room temperature. It is suggest that complications due to malaria infection can be greatly profounded with high testosterone levels in males. Moreover, these effects can also be worste when subjects are exposed to heat stress.
URI: http://khartoumspace.uofk.edu/handle/123456789/20054
Date: 2016-03-24


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