effect of an organophosphorous insecticide on the hepatic, renal and pulmonary tissues of mice fetuses

The present study deals with the effects of the organophosphorous insecticide curacron on the hepatic, renal and pulmonary tissues of mice fetuses. Fourty pregnant females were divided into four groups, 10 individuals each. The 1st group served as control group. The individuals of the 2nd and 3rd groups were given oral dose of curacron 14.4 and 28.8 mg/kg, respectively on day 7 of gestation. The 4th group was given 14.4 mg/kg for 8 successive days from day 7 to day 14 of gestation. At the 18th day of pregnancy, females from both the control and treated groups were sacrificed and samples of hepatic, renal and pulmonary tissues were taken from the fetuses. The liver of the 18-days-old fetuses of all experimental groups showed different phases of venous congestion, disorganization of the hepatic lobules, fatty degeneration and necrosis. The kidney of curacron-treated groups showed venous congestion, cloudy swelling, and necrosis of the epithelial cells lining the kidney tubules. Moreover, the lungs of the different treated groups showed dilation and congestion of the blood vessels, thickening of the interalveolar septa and scattered cell debris in the lumens of the alveoli. Consequently, cumulative doses of curacon obviously affect hepatic, renal and pulmonary fetal tissues and extreme caution should be considered by pregnant women to avoid its hazardous effects on their fetuses

effect of losartan on the kidney of adult female albino mice and on the renal, hepatic and pulmonary tissues of their fetuses

Angiotensin receptor blockers as well as angiotensin-converting enzyme inhibitors are antihypertensive medications prescribed by a wide variety of physicians. Blocking of angiotensin II [ANG II] mainly through angiotensin II type I receptor [AT[1]] has been implicated in mediating the angiotensin-converting enzyme [ACE] inhibition. The present study was designed to investigate the effects of an AT[1] antagonist, losartan, on the renal tissues of adult and fetus as well as the hepatic and pulmonary tissues of fetuses histologically and ultrastructurally. Pregnant CD-1 mice were used in this study and they were administered losartan orally through gastric tube. Animals were divided into three groups; the first group served as control, while the second and third groups were administered losartan [10 mg/kg/day] during the second and third weeks of pregnancy respectively. At the end of pregnancy, the pregnant females were sacrificed and the fetuses were removed where the kidney of both adult and fetuses as well as the liver and lung of fetuses were removed. Light and electron microscopic examination of the selected tissues revealed conspicuous pathological lesions especially in the second group. Renal lesions were represented by hypertrophied glomeruli with a marked increase in mesangial cells, interstitial fibroblasts proliferation and haemorrhage. Ultrastructural changes were represented by thickening of the glomerular basement membrane, fusion of foot processes and tubular necrosis in both adult and fetuses. Moreover, the fetal liver of the second group showed marked accumulation of glycogen contents, fatty degeneration, necrosis and nuclear pyknosis. The fetal lung revealed remarkable damage of the epithelial cells lining the respiratory bronchioles, focal areas of cellular necrosis, moderate increase in pneumocytes type II and macrophages. A marked increase in number of alveolar fibroblasts was also observed. Consequently, such pathological lesions induced by losartan-treatment might lead to renal dysfunction, hepatic injury and chronic lung inflammation. Thus, extreme caution seems to be necessary in losartan treatment during pregnancy. It is essential to balance the risks of toxicity from drug treatment, the hazards of the fetus against the risks of non treatment during the second trimester of pregnancy

Scanning and transmission electron microscopic studies of the traechea and lung in nicotine treated rats

In the present investigation, the morphological and ultrastructural alterations in both trachea and lung of rat following nicotine treatment were studied using scanning and transmission electron microscopy. Adult male albino rats, injected subcutaneously with a high dose of nicotine [25 mg/kg body weight] for 15 successive days, were used in the present study. Nicotine induced extensive morphological and ultrastructural changes in both trachea and lung tissues. The respiratory epithelium of trachea changed to stratified squamous form with a remarkable increase in goblet cells. Moreover, the loss and destruction of cilia in most of the ciliated columnar epithelium and the increase of brush cells in nicotine treated rat mucosa were also detected. Marked thickening of the interalveolar septa, lymphatic infiltration and degenerated cells were observed in lung tissue. Type II pneumocytes with an increase in surfactant bodies, necrotic cells, cell debris and macrophages, together with a marked increase in the thickness of collagen fibers were revealed in the lung tissue. Furthermore, necrotic cells with degenerated cellular organelles were observed in both trachea and lung tissue. In conclusion, nicotine is considered as a toxicant with a unique progression of injury