effects of 900-Mhz-emitted mobile phone on the uterus and ovaries of albino female rats

This work was done to study the effects of exposure to mobile emits 900MHz electromagnetic field [EMW] on the uterus and ovaries of female rats. Thirty female adult rates were randomly divided into three groups [10 each] as follows: negative control group [1], positive control group [II]: without exposure to electromagnetic wave [exposure device off for 30 min/day for 30 days]. Exposure group [III]: exposed to 900MHz electromagnetic wave [EMW] for 30 min/day for 30 days. The results showed a significant reduction in ovarian weights and non significant change in uterine weight in the exposed rats [group III] when compared to the other control groups. The Serum levels of estrogen and progesterone were significantly decreased among EMW exposed group. Ovarian and endometrial tissue homogenate revealed a significant increase in malondialgehyde [MDA] levels, while they showed a significant decrease in the activity of the reduced gluthathione [GSH] in the same group. In the EMW exposed group, histopathological changes revealed many apoptotic cells with densely stained cytoplasm and fragmented or phyknotic nuclei, in the endometrial surface, epithelial and glandular cells. The glands were significantly decreased in number and diffuse inflammatory cell infiltration were observed in the endometrial stroma. Sections of ovaries revealed significant decrease in the follicle numbers in EMW exposed group III compared to both control groups. Uterine sections immunolabeled for active caspase-3, showed significant increasing in numbers of immunolabeled cells for activated caspase 3 and apoptotic cells, in EMW-exposed group III. In conclusion, this study demonstrated that there is impairment in endometrial and ovarian tissues both at biochemical and histological levels after experimental exposure to 900-MHz emitted mobile phone

Effect of ascorbic acid on aflatoxin B[1] induced chronic hepatotoxicity: an experimental study

This study was done to evaluate the effect of chronic Aflatoxin B[1] [AFB[1]] administration on the liver of albino rats and to investigate the role of ascorbic acid as a protective agent. It was carried out on 90 male adult albino rats weighing 150-200 gms and divided into 6 numerically equal groups each group consists of 15 rats. First group [-ve control group] untreated animals, second group received olive oil, third group received ascorbic acid, fourth group received distilled water. Both second, third and fourth groups were served as +ve controls. Fifth group received AFB[1] and sixth group received ascobic acid prior to AFBJ. After 12 weeks of treatment all animals were sacrified and blood was collected to investigate the liver functions [ALT, AST, serum billirubin and alkaline phosphatase]. Liver sections of different groups were examined histopathologicaly using light microscope. The results revealed that the levels of liver functions in AFB[1] group were significantly higher than the control groups. In rats which received ascorbic acid prior to AFB[1], the levels of liver functions were significantly reduced to more or less the levels of the control groups. Light microscopic examination of the control groups demonstrated the normal hepatic structure. Histopathological examination of liver specimens of AFB[1] treated rats group showed vacular degeneration, focal necrosis, fatty changes, kupffer cell hyperplasia and portal infiltration and these harmful effects were reduced in rats group treated by ascorbic acid prior to the administration of AFB[1]. In conclusion this work showed that liver damage of rats treated with AFB[1] is associated with biochemical elevation of liver functions and confirmed by histopathological changes. Ascorbic acid can be considered as a potential antidote against the harmful effect of AFB[1] on liver

Tin Chloride pretreatment prevents potassium dichromate induced nephrotoxicity and Ischemic acute renal injury in rats

This study was done to investigate whether tin chloride [Sncl[2]] pretreatment ameliorates renal injury in rats with toxic or ischaemia acute renal failure [ARF]. It was carried out on 100 adult male albino rats weighing 180-220 gm. Rats were divided into 5 numerically equal groups [each contains 20 animals]. Control group [received physiological saline] group pretreated with physiological saline before single subcutaneous[S.C.] injection of potassium dichromate [K[2]Cr[2]O[7] in a dose of 25 mg/kg, group treated with Sncl[2][10 mg/100 g BW, subcutaneously] 12 hours before K[2]Cr[2]O[7] and group subjected to renal ischaemia. The group of renal ischaemia were subdivided into 2 groups: pretreatment with the same volume of physiological saline 24 hrs before ischaemia and pretreatment with Sncl[2] [10 mg/100g Bw, subcutaneously] 24 hrs before ischaemia,. After the desired period of treatment, animals were killed at different intervals of time. Blood was collected to investigate the renal functions [bloo urea nitrogen and serum creatinine], and kidneys wer examined histopathologically. The results revealed that, K2Cr2O7 and renal ischaemia markedly increased renal functions. Histological sections of ARF treated rats revealed an extensive tubular cell necrosis. Tin chloride pretreatment which specifically induced renal heme oxygenase activity in the rat ameliorated the toxic and ischaemia renal i njury as judged by the significant decrease in serum creatinine and blood urea concentrations and the lesser tubular cell injuries