11 research outputs found

    Stress induced alterations in pre-pubertal ovarian follicular development in rat

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    The objective of the study was to find out whether stress experienced during neo-natal period alters the timing of formation of pre-antral and antral follicles and if so, whether pre-treatment with CRH receptor antagonist prevents these effects in rats. New born rat pups (n= 15) were exposed to maternal separation (6 hours/ day) from post-natal day (PND) 1 to 7 and were killed on PND 8, 11 and 15. The time of exposure was randomly changed every day during light phase (7Am to 7Pm) of the day to avoid habituation. There was a significant increase in serum corticosterone levels on PND 8 and 11 in stress group rats compared to controls indicating stress response in these pups. The ovary of both control and stressed rats contained oocytes and primary follicles on PND 8 and 11 and in showed progress of follicular development upto to pre-antral and early antral follicle formation on PND 11 and 15. However, mean number of healthy oocytes and all categories of follicles at all ages studied were significantly lower in stressed rats compared to controls. Concomitant with these changes, number of atreatic follicles showed an increase over control values in stressed rats. The increase in atresia of follicles was due to apoptosis as shown by increase in the percentage of granulosa cells showing TUNEL positive staining and caspase 3 activity. On the other hand, pre-treatment with CRH- receptor antagonist (CRH 9-41) 2ng/ 0.1 ml/ rat prior to undergoing stress regime on PND 1 to 7, prevented alterations in pre- pubertal follicular development thereby indicating that the ovarian changes were due to effects of stress induced activation of HPA axis. The results indicate that, stress during neonatal phase, though does not affect timing of formation of pre-antral and antral follicles, it does enhance atresia of follicles of all categories, including follicular reserve, which may affect the reproductive potential of adults. The results, for the first time reveal that CRF receptor antagonist prevents pre-pubertal ovarian stress response

    Reduced antioxidant status for prolonged period due to repeated stress exposure in rat

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    The objective of the study was to find out whether or not exposure to a stressor after an initial stressful experience augments stress response. Antioxidant status was determined by measuring changes in the activities of the hepatic free radical scavenging enzymes viz, superoxide dismutase (SOD), glutathione-S-transferase (GST), glucose-6-phosphate-dehydrogenase (G6PDH) and catalase (CAT) and levels of hepatic malondialdehyde (MDA) following exposure to 1 h restraint (RS) and after a gap of 4 h to forced swimming exercise (FS) in rats. The activities of hepatic CAT, SOD, G6PDH and GST were significantly reduced 2 h after RS compared to controls and 4 h after FS the activities of CAT and G6PDH remained at lower levels i.e. they were similar to those found after RS , whereas SOD and GST showed further significant decrease compared to those found after RS. On the other hand the MDA levels, indicative of lipid peroxidation were significantly increased after RS and showed further significant increase after FS. The results reveal that after initial stressful experience, the stress response is augmented due to exposure to another stressor whereas the system does not get habituated to stress exposure

    Influence of Corticosterone on FSH-Induced Ovarian Recrudescence in the Lizard Mabuya carinata

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    Administration of bovine FSH (10 IU/lizard/alternate day for 30 days) in the postbreeding quiescent phase of the ovarian cycle caused a significant increase in the mean number of oogonia and oocytes, the relative weight of the oviduct, and the liver and serum estradiol levels compared to those of controls. In addition, the FSH-treated Lizards showed a vitellogenic growth of follicles and development through to preovulatory follicles. However, the administration of corticosterone simultaneously with FSH (10 IU FSH + 40 mu g corticosterone/lizard/alternate day for 30 days) did not result in these changes and the ovaries resembled those of controls. The results indicate the absence of ovarian refractoriness to gonadotropic stimulation during the quiescent phase of the reproductive cycle and inhibition of FSH-induced ovarian recrudescence by corticosterone. It is suggested that corticosterone treatment reduces FSH-induced steroidogenic activity of the ovary, leads to impairment in vitellogenin secretion by the liver, and results as well in the failure of vitellogenic follicular growth in Mabuya carinata. (C) 1999 Academic Press

    Effect of cypermethrin on the ovarian activity and its impact on fertility and pubertal onset of offspring

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    Oral (by gavage) administration of cypermethrin (CYP), (3 doses; 1.38, 2.76 and 5.52 mg/kg body weight) to female mice for two durations (6 weeks and 12 weeks), caused significant reduction in the number of estrous cycles per month, serum levels of estradiol, total number of healthy ovarian follicles and number of corpora lutea whereas there was an increase in number of atretic follicles of all categories compared to controls. Mice of all treated groups after 6 weeks treatment showed 100% fertility. It was 80% in low and medium doses and 60% in high dose treatment after 12 weeks. There was a significant delay in the onset of puberty and reduction in number of estrous cycles of progeny of medium and high dose CYP treated mice mated with normal males. Number of estrous cycles per month, healthy follicles, corpora lutea and serum levels of estradiol, were not reversible within 6 weeks after cessation of medium and high dose treatment for 12 weeks. The study first time reveals that reversibility of the reproductive toxic effects of CYP depends on quantum and duration of exposure. Keywords: Cypermethrin, Pyrethroid, Fertility, Estrous periodicity, Estradio

    Chronic stress induced duration dependent alterations in immune system and their reversibility in rats

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    The objective was to find out whether severity of stress effects on immunity increases with duration of exposure and recovery depends on duration of exposure. Adult male rats (n = 30) were subjected to restraint (1 h) followed by forced swimming exercise (15 min) after a gap of 4 h daily for 2, 4 and 8 weeks and allowed to recover for 6 weeks after each exposure period. Exposure of rats to stress resulted in duration dependent significant decreases in leukocyte count, phagocytic indices of neutrophils, number of bone marrow stem cells and serum levels of IL-12 and increases in apoptotic index of peripheral blood mononuclear cells and serum levels of IL-10. The alterations in counts of neutrophils, total immunoglobulin content, phagocytic index, apoptotic index of peripheral blood mononuclear cells and serum levels of IL-10 returned to control levels in recovery group rats of 2 and 4 weeks exposure but not in that of 8 weeks exposure. However, alterations in number and apoptotic index of bone marrow stem cells returned to control levels in 2, 4 and 8 weeks stress recovery groups. The results for the first time reveal that increase in duration of exposure results in more severe damage in immune system and that shorter the exposure period, faster the recovery. In addition, in vitro study for the first time showed that corticosterone causes apoptosis of peripheral blood mononuclear cells and bone marrow stem cells in dose dependent manner. Hence death of leukocytes and their stem cells is the major cause of stress induced immune dysfunction
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