Immunohistochemical study of male albino rat prostate in different age groups after castration

In this study we examined the lobe-specific and age-dependent expression of Bcl-2 and Bax proteins, 80 male albino rats were used in this study, 20 rats were control 10 aged 4 month, and 10 aged 24 months, the rest of animals were divided into 3 equal groups each 20 animals half of them 4 months age and the rest 24 months age. The experimental groups were castrated, and were killed at 1, 10, 30 days after castration. Bcl-2 expression in the ventral lobe were lower compared with expression in the dorsal and lateral lobes respectively. Bax expression in the ventral lobe was higher than that in the lateral and dorsal lobes, respectively. In all three lobes, Bcl-2 was detected in epithelial cells, but not in stromal cells, where as Bax. protein was localized in both cell types. After castration, Bcl-2 expression in the ventral lobe decreased significantly from the control level shortly after castration, but increased significantly by 30 days. By contrast, Bax expression increased significantly, gradually decreased by time, and was nearly undetectable by 30 days post-castration. In the dorsal and lateral lobes, neither Bcl-2 nor Bax expression was significantly altered after castration. In the ventral lobe of old rats after castration, Bcl-2 followed a pattern of expression similar to that observed in young rats. However, Bax were lower in old rats compared with those in young rats after castration. Therefore, cell death follows the down-regulation of Bcl-2 expression in the ventral lobe of young and old rats. Moreover, the higher Bcl-2 expression in the dorsal and lateral lobes of controls and in the ventral lobe by 30 days after castration serve to protect cells from apoptosis. The conclusion of the study was that; the rat prostate lobes offer a model to study the molecular mechanisms of cell death and survival that are related to the androgen dependence of prostate epithelial ceils in normal and diseased conditions. The relative abundance of Bcl-2 and Bax proteins is critical in directing cells toward or away from apoptosis. The relative abundance of Bcl-2 protein correlates with the survival of prostatic epithelial cells. The age dependent decrease in cell death correlates with a reduced stimulation of Bax protein

Effect of desferoxamine and urine alkalinization on myoglobin-induced kidney injury in albino rats

Myoglobinuric acute renal failure is a known complication of several clinical sittings involving muscle damage. Renal damage has been partially attributed to iron released from myoglobin, which then catalyzes the generation of reactive oxygen species and oxidant tissue injury. To define whether desferrioxamine [iron chelator] and urine alkalinization would confer direct and additive protective effects on myoglobin-induced renal failure, glycerol model of myoglobinuric acute renal failure in albino rats was used. Rhabdomyolysis was induced by injecting hypertonic glycerol solution in saline [50%], at a dose of 8 ml/kg body weight, in the muscles of the hind limbs of rats. Forty adult male rats were randomized into five groups, eight rats/group. The 1st group was injected with glycerol solution, the 2nd with glycerol and intra-peritoneal desferrioxamine at a dose level of 50 mg/kg body weight twice daily, the 3rd with glycerol and given 0.28 molar sodium bicarbonate drinking solution, the 4th with glycerol and desferrioxamine and was given the alkali drinking solution, and the 5th [control group] with normal saline and desferrioxamine and given the alkali drinking solution. The results showed that desferrioxamine and urine alkalinization reduce oxidative stress in renal tissue and protect against functional and structural myoglobinuric renal damage, and both treatment regimens provide additive protective effects