Postnatal changes in the development of rat submandibular glands in offspring of diabetic mothers: Biochemical, histological and ultrastructural study.

Development and maturation of submandibular salivary glands are influenced by intrauterine diabetic environment. Several studies investigated the effects of diabetes on the salivary glands. However, the effects of maternal diabetes on the submandibular glands of the offspring was not properly examined. Therefore, the present study was designed to describe the changes in the development of the submandibular glands of the offspring of diabetic mothers. The submandibular glands of the offspring of Streptozotocin (STZ)-induced diabetic female rats were examined at two and four weeks after birth. Detection of mRNA demonstrated that maternal diabetes affects the level of different indicators. The reduction of expression of epidermal growth factor (EGF); a protein mitogen, cytokeratin 5 (CK5); an epithelial cell progenitor, CK7 and aquaporin 5 (AQP5); differentiation markers and B cell lymphoma 2 (Bcl2); an antiapoptotic marker were found. Increase in Bcl2-associated X protein (Bax); an apoptotic marker was detected. These changes indicate their effects on saliva secretion, glands tumorigenesis, growth of normal oral flora and oral microbes, with decreased protein synthesis and production of xerostomia and dental caries. Loss of normal glandular architecture, significant increase in fibrosis, by the detection of collagen fibers, and stagnation of secretory granules were found with atrophic changes in the acinar cells. Marked defect of polysaccharides in the acinar cells, denoting functional changes, was manifested by significant reduction of the intensity of periodic acid-Schiff (PAS) reaction. The positive immunoreactivity of caspase-3, denoting cellular apoptosis, and minimal reaction of alpha-smooth muscle actin (α SMA) and proliferating cell nuclear antigen (PCNA) were evident in the offspring of diabetic mothers. We conclude that maternal diabetes produces degenerative effects in the structure and function of the submandibular salivary glands of the offspring, reflecting possible influences on their secretory activity affecting oral and digestive health.

Concomitant protective and therapeutic role of verapamil in chronic mercury induced nephrotoxicity in the adult rat: histological, morphometric and ultrastructural study.

INTRODUCTION: Mercury intoxication is a widespread problem as mercury is used in the manufacture of thermometers, batteries and electrical switches. It forms one of the most diffusible environmental pollutants. Mercury has a nephrotoxic effect which could occur at low exposure levels. Verapamil could help in the treatment of mercuric toxicity. The aim of the study was to examine the protective and therapeutic effect of concomitant verapamil on chronic mercuric chloride nephrotoxicity. This was done through histological, morphometric and transmission electron microscopic studies. MATERIAL AND METHODS: Sixty adult male albino rats were used. The rats were divided into a control group and 4 experimental groups: group I (HgCl2), group II (concomitant HgCl2 and verapamil), group III (HgCl2 withdrawal) and group IV (HgCl2 withdrawal then verapamil treatment). RESULTS: Chronic administration of HgCl2 resulted in cortical nephrotoxic effects in the form of glomerular sclerosis, acute tubular necrosis and interstitial inflammatory cellular infiltration which eventually ended in interstitial fibrosis. Concomitant use of verapamil with HgCl2 improved the previous pathological changes partially. The findings in group III were less severe compared to group IV. The persistence of the pathological findings in these groups reflects the irreversible nephrotoxic changes caused by chronic HgCl2 exposure. CONCLUSIONS: We concluded that the concomitant administration of verapamil has a much better effect in minimizing the nephrotoxic effect caused by chronic HgCl2 than its therapeutic administration. So, we recommended the prophylactic use of verapamil in suspected cases of chronic mercuric chloride nephrotoxicity to preserve renal function.