Histological and immunohistochemical analysis of BCL-2 and P 53 experession in relation to apoptosis in normal, benign and malignant human female mammary gland epithelium

Apoptosis is a genetically regulated form of programmed cell death. It occurs in response to physiological stimuli and secondary to cell injury and stress. It has a role in the regulation of cell population density during embryogenesis, aging and in many diseases. This work was performed to study the expression of the apoptosis -related proteins [Bcl-2 and P53] in normal human female mammary gland epithelium at different physiological stages [puberty, lactation and involution] and in breast fibroadenoma and invasive breast carcinoma. Breast specimens were processed for histological, immunohistochemical and statistical studies, Histologicaly, most of the apoptotic cells showed shrunked cytoplasm and fragmented nuclei and were seen predominantly in the basally located glandular epithelial cells. Different patterns of Immunoreactivity for Bcl-2 and p53 was present throughout the mammary epithelial cells, suggesting different grades of susceptibility towards apoptotic stimuli in individual glandular epithelial cells. However, specific cells showed strong reaction for Bcl-2 and P53. Specific Bcl-2 and p53 expression patterns could reflect particular cell differentiation states. Bcl-2 and P53 expressions are associated with prognostic histopathological features and their evaluation is of value in predicting the clinical course and the programs of treatment of b

Possible reversible action of phenobarbital of the liver of the albino rat

Three groups of rats were used in this experiment, a control, a phenobarbial-treated and a reversible group. Each animal in the control group received 80 mg/kg body weight of saline intraperitonal. Each animal in the phenobarbital-treated group received 80 ml/kg body weight of phenobarbital intraperioneally for 5 days. Animals of the reversible group were left one weak after receiving the same dose of the drug as the treated group. Daily measurements of body weight were performed and liver weight was calculated in the day of sacrifice. Enzymatic liver glycogen determination. PAS staning and electron microscopic studies of liver cells were done. The results shows that phenobarbital causes reduction in the body weight with increase in the liver weight. Proliferation of smooth endoplasmic reticulum was found to be the main factor reponsible for the increase in liver weight. The drug affects all the three zone of the hepatic lobule with particular ultrastructural patter in each zone. There was an increase in lipid droplets deposition mainly in the midlobular zone. All changes in the body weight, liver weight, glycogen content and ultrastructure were reversible after one week of cessation of phenobarbital treatment