Catalase in testes and epididymidis of wistar rats fed zinc deficient diet.

Catalase activities have been evaluated in testes and caput and cauda epididymis of Wistar rats fed on zinc deficient diet for 2 and 4 weeks. The enzyme activity has been measured as chromic acetate formed by heating of dichromate (in acetic acid) in presence of H(2) O(2) with perchromic acid as an unstable intermediate. Observed non-significant increase in catalase activity in testes as well as in caput and cauda epididymis of 2 weeks experiments has been related to low levels of H(2) O(2) produced in two organs whereas significant (P<0.01/0.001) increase in catalase activity in 4-weeks experiments indicate for increased oxidative stress due to phagocytotic activity of Sertoli cells in testes and damaged spermatozoa in epididymis. Thus, zinc deficiency increases catalase activity in testes and epididymis.

Short-term zinc deficiency in diet induces increased oxidative stress in testes and epididymis of rats.

In order to determine the effects of Zinc deficient diet on oxidative stress in testis and epididymis, various parameters viz: total proteins, lipid peroxidation, hydroperoxides, antioxidant capacity and enzymatic activities are evaluated in rats fed on zinc deficient diet for 2, 4 and 6 weeks. Total proteins, water and lipid solouble antioxidant capacity decreased while lipid peroxidation (TBARS) and hydroperoxides concentration increased in testes, caput and cauda epididymis except in 2ZD (testes) where hydroperoxides revealed a significant decrease. GSH decreased in testes and caput and cauda epididymis. GPx and gamma-GT activities increased in testes and caput and cauda epididymis of zinc deficient rats. Further, GST increased in testes but exhibited decreases after 2 and 4 weeks and an increase after 6 weeks in caput and cauda epididymis of zinc deficient rats. GR activities decreased in testes but it increased in caput and cauda epididymis of zinc deficient rats. Thus, zinc deprivation results in increased sensitivity to oxidative stress. All these may have been as a consequence of increased ROS generation and/or decreased zinc dependent antioxidant processes.

Antioxidative effect of Rajgira leaf extract in liver of Swiss albino mice after exposure to different doses of gamma radiation.

The radioprotective effect of Rajgira leaf extract (800 mg/kg b.wt.) was studied in the liver of Swiss albino mice at various post-irradiation intervals between day 1 and 30 after its oral administration for 15 consecutive days prior to whole body gamma irradiation with 6, 8 and 10 Gy of gamma rays. In this study, abnormal and binucleated hepatocytes were counted in both the control and experimental sets because these hepatocytes are good indicators of radiation-induced damage. In the experimental (RLE + irradiation) sets, the percentage of abnormal and binucleated hepatocytes was lower compared with their respective control (irradiation alone) sets at each autopsy interval with all three radiation doses studied. The increase in the percentage of these hepatocytes was also found to be dose-dependent in the control as well as in the RLE treated (experimental) sets. Thus, Rajgira leaf extract (RLE) treatment given before irradiation protects mouse liver against radiation-induced lesions by increasing the GSH content and decreasing the LPO level.

Radiomodulatory influence of Rajgira (Amaranthus paniculatus) leaf extract in Swiss albino mice.

Radiomodulatory effect of Rajgira leaf extract against 6, 8 and 10 Gy gamma radiation has been evaluated by 30 day survival of Swiss albino mice. Animals of control groups (untreated irradiated) showed diarrhoea, ruffled hairs, epilation, facial edema and consistent decrease in body weight. These signs were less severe/absent in experimental groups (Rajgira treated irradiated), and recovery in body weight was also early and faster. Thirty day survivability was 66 per cent in control group, exposed to 6 Gy, whereas no animal survived beyond 14 and 10 days after irradiation with 8 and 10 Gy gamma rays respectively. However, 100, 60 and 25 percent survivability was observed in experimental groups at 6, 8 and 10 Gy respectively. Regression analysis of survival data showed that the LD50/30 values were 6.33 and 8.62 Gy for control and experimental animals respectively. The dose reduction factor (DRF) was computed as 1.36. A significant decrease in GSH content and increase in LPO level was observed in control animals, whereas in Rajgira pretreated irradiated animals the level of GSH was recorded significantly higher but LPO level decreased significantly. The results from the present study suggest that Rajgira pretreatment provide protection against gamma irradiation in mice.

Mentha piperita (Linn) leaf extract provides protection against radiation induced alterations in intestinal mucosa of Swiss albino mice.

Intestinal protection in mice against radiation injury by M. piperita (1 g/kg body weight/day) was studied from day 1 to day 20 after whole body gamma irradiation (8 Gy). Villus height, goblet cells/villus section, total cells, mitotic cells and dead cells/crypt section in the jejunum are good parameters for the assessment of radiation damage. There was significant decrease in the villus height, number of total cells and mitotic cells/crypt section, whereas goblet cells and dead cells showed significant increase after irradiation. Mentha pretreatment resulted in a significant increase in villus height, total cells and mitotic cells, whereas goblet cells and dead cells showed a significant decrease from respective irradiated controls at each autopsy day. The results suggest that Mentha pretreatment provides protection against radiation induced alterations in intestinal mucosa of Swiss albino mice.

Embryonic/fetal mortality after exposure to tritiated water in pregnant Swiss albino mice during different gestation periods.

Pregnant Swiss albino mice were given a priming injection(im) of tritiated water (HTO) at the dose rate of 2.3 and 5 microCi/ml body water (74, 111 or 185 KBq/ml body water) at 0, 6 and 14 day post conception (d.p.c.) and were subsequently maintained on tritiated drinking water ad libitum during preimplantation (0-5 d.p.c.), organogenetic (6-12 d.p.c.) or fetal (14-18 d.p.c.) period, respectively. On day 18 of gestation the females were sacrificed by cervical dislocation to record the implant sites per dam and embryonic/fetal mortality. Significant reduction was observed in average implant sites per dam when the females were exposed to any of the three doses during the preimplantation period due to embryonic resorption before implantation. However, the same was found to be within the normal range when mothers were exposed during the organogenetic or fetal period. Prenatal mortality (embryonic resorption/fetal death) was higher after in utero exposure to different doses during preimplantation period as compared to organogenetic period, but mortality did not occur after exposure to any of the doses during the fetal period. Occurrence of mortality was found to be dose dependent.

MPG protection against radiation sickness and weight loss and its correlation with mortality of mice after whole-body gamma-irradiation.

The radiation-induced mortality together with the loss of body-weight and development of radiation sickness was studied in young adult Swiss albino mice after exposure to 1500 R of 60Co gamma-radiation in the presence and absence of 2-mercaptopropionyl-glycine (MGP), and results from both the groups were compared. It was found that the time of onset of radiation sickness was delayed in the drug-treated group, the mean survival time was also increased to 6 days as compared to 4.5 days in the untreated control group. These changes showed a direct correlation with the body-weight changes as the loss of weight in the drug-treated group was less marked and more gradual than in the untreated controls.

Radiation protection of pronormoblasts and normoblasts by 2-mercaptopropionylglycine (MPG).

The pronormoblasts and normoblasts in Swiss albino mice were found to be very sensitive to radiation and their percentage was reduced drastically after exposure to gamma-rays. The degree of damage increased with increase in radiation dose. MPG reduced the initial damage and brought about an early and fast recovery. It is concluded that the drug protects the stem cells and thereby reduces the depletion of the regenerating pool which causes a more efficient and accelerated recovery.

Modification of radiation-induced spleen weight changes in mice by 2-mercaptopropionylglycine.

It was found that the MPG partially protects the spleen against weight loss due to radiation, and exaggerates the compensatory reaction in the tissue during recovery. It is also concluded that MPG protects the stem cells in the spleen, which helps to restore the peripheral blood by extramedullary erythropoiesis.

MPG protection and goblet cell kinetics in mouse jejunum.

Experiments were undertaken to study the goblet cell changes in the jejunum of mice irradiated in the presence and absence of the protective drug 2-mercaptopropionylglycine (MPG). One group of adult Swiss albino mice of 6 to 8 weeks was injected with the drug (MPG) intraperitoneally and a second group was injected with distilled water in the same manner and served as a control. 15-30 minutes after injection animals from both the groups were exposed to a Co-60 source to give a total dose of 1000 R at the rate of 25 R/min. Three animals from each group were sacrificed at different successive intervals. 5 micron paraffin sections of the jejunum were prepared and goblet cells were counted in the crypt and villus region. The results from the two groups were compared. The results from MPG treated mice indicated that there was a protection from the radiation-induced changes. The drug accelerated the regeneration process leading to the restoration of normal number of goblet cells by the last interval studies.