Genotoxicity of cadmium in rat lung cells assessed by an alkaline comet assay and the possible protective role of selenium

Cadmium is a highly toxic heavy metal with many hazardous effects. Selenium is an essential trace element with antioxidant properties. To evaluate the cadmium-induced DNA damage in rat lung cells and the possible protective role of selenium. Thirty-six adult male albino rats were used in this experiment. They were divided into four equal groups. Group I was the control group. Group II included rates that were injected intraperitoneally with cadmium chloride [CdCl[2]] [1.0 mg/kg/day] for 8 weeks. Group III included rates injected intraperitoneally with sodium selenite [Na[2]SeO[3]] [0.25 mg/kg/day] for 8 weeks. Group IV included rats injected intraperitoneally with both CdCl[2] [1.0 mg/kg/day] and Na[2]SeO[3] [0.25 mg/kg/day] for 8 weeks. At the end of the experiment, the lungs of rats were taken and processed for single-cell gel electrophoresis [comet assay]. In the control group, comets appeared with large bright heads and small tails. The injection of CdCl[2] in group II induced DNA damage in rat lung cells, indicated by increased migration in the comet assay. Comet cells appeared with small heads and long tails. Statistically, there was a significant increase in tail length, tail moment, and tail% DNA compared with the control. Injection of selenium alone did not show any difference from the control. Concomitant administration of both cadmium and selenium resulted in a partial decrease in the DNA damage in rat lung cells indicated by decrease in DNA migration in the comet assay. Comet cells appeared with large heads and relatively small tails compared with those of group II. A significant decrease was also observed in tail length, tail moment, and tail% DNA compared with group II. CdCl[2] could significantly induce DNA damage in rat lung cells. It was suggested that selenium could partially ameliorate DNA damage induced by cadmium

Histological and immunohistochemical study on the effect of hypo and hypercaloric diet on the structure of hippocampus of male albino rat

Caloric restriction remains the major, non genetic intervention that extends the life span of the short and long -lived mammalian species. This nutritional intervention also delays the onset, or slows the progression of many age-related disease processes. The present study investigated the effect of hypocaloric diet, in comparison to the hypercaloric and the balanced diet feeding on the structure of hippocampus. The study was conveyed on young and aged male albino rats for eight weeks. Showed that the aged control rats manifested many degenerative changes in the hippocampus. These changes were in the form of degenerated pyramidal cells with pyknotic nuclei and Karyolysis of some cells. A significant decrease in the pyramidal cell number was detected with a significant compensatory increase in the number of the astrocytes. Shrinkage of some pyramidal cells and swelling of others could be observed. Hypercaloric diet feeding resulted in exaggeration of these age -related changes that started to be noticed in the young rats. On the other hand hypocaloric diet feeding attenuated the age-related hippocampal changes. This was evidenced by histological, immunohistochemical, and statistical studies. These results direct our attention to limit the caloric intake in our food, to maintain a healthy life style for safe aging

Intrahepatic bile duct development in the human foetus

This study included twenty human foetuses during various periods of gestation ranging from 9 to 40 weeks. The age of the foetus was approximately determined. Specimens from the liver were obtained and subjected to the appropriate histological and histochemical techniques. The data revealed that the bile duct system was immature at 9 weeks-old foetuses. Then at the 11th week, groups of hepatic cells were arranged in close contact with portal vein branches. At 12 weeks-old foetuses, the biliary ducts started to appear as small spaces among these groups of hepatic cells. At 18 to 20 weeks, portal spaces became obvious and duct-like structures were observed in the parenchyma-connective tissue contact area around these portal spaces. From the 21st week onwards, developing biliary structures were observed at the margins of the portal spaces. Then the portal mesenchymal tissue successively surrounded the bile ducts and pushed them inside portal spaces. At week 40, the number of large individual bile ducts increased in each portal area. The present results suggested that the cells lining the developing biliary structures originated from the hepatoblasts. The number of ductular structures per portal tract increased in full term foetal liver. Nevertheless, the bile canalicular system was less conspicuous till the full term gestational period suggesting that development will continue in the postantal life