Response of liver antioxidant defense system to acute and chronic physical and psychological stresses in male rats

The aim of this study was to evaluate the effect of acute and chronic physical and psychological stressors on the induction of oxidative stress in male rat liver. Male Wistar rats were randomly divided into 3 groups as following: control, physical and psychological stress groups. Stress was induced by communication box for one (acute), fifteen and thirty (chronic) days. Once stressor periods ended, rats were anesthetized and their liver dissected out for later assessments. Exposure to physical stress enhanced liver superoxide dismutase (SOD) (19.44 %) and glutathione S-transferase (GST) (21.84 %) activities and decreased glutathione (GSH) (30.03 %) level on the 1st day (p<0.05). SOD (24.13 and 18.43 %) and GST (27.77 and 21.27 %) activities were significantly increased, while catalase activity (29.74 and 24.41 %) and GSH level (35.05 and 31.05 %) were decreased in psychological stress group after 1 and 15 days (p<0.01 and p<0.05) compared to the 1st day value in control group, respectively. Psychological stress induced an increase in liver malondialdehyde (MDA) (46 %) and plasma corticosterone (36 %) levels on the 1st day (p<0.05). However, all parameters returned to their basal value after 30 days of stress. The results suggest that exposure to acute physical and psychological stressors induce the production of reactive oxygen species and oxidative stress in rat liver due to GSH depletion and the decreased catalase activity. The elevation of lipid peroxidation and corticosterone level in acute psychological stress may lead to more profound oxidative damage than acute physical stress. Moreover, cell protection in hepatic tissue of chronically stressed rats is indicative of possible late adaptation of the animals to stress

Early postnatal hypothalamic-pituitary-adrenal axis activity and reduced insulin sensitivity in adult rats

Objective. Early life stress influences the development of metabolic disorders, including functional changes in the developing of pancreas mediated hypothalamic-pituitary-adrenal (HPA) axis. In the present study, the role of an early postnatal stress on corticosterone, glucose, and insulin levels was investigated during young adulthood

Histological Evaluation of Pancreas Following Early Life Stress in Exposure to Pubertal Stress in Male Rats

Background and purpose: Stressful events in early-life induce metabolic disorders in adolescence. The aim of this study was to investigate the effect of early-life stress on number or area of Langerhans islets in exposure to foot-shock and psychological stress in male rats. Materials and methods: The rats were divided into six groups: control (without stress), early-stress (stress at 2 weeks of age), pubertal-foot shock (at 8-10 weeks of age), pubertal-psychological stress (psychological stress at 8-10 weeks of age), early-stress + pubertal-foot shock (stress at 2 weeks and foot-shock at 8-10 weeks of age), early-stress + pubertal-psychological stress (early-stress at 2 weeks and psychological stress at 8-10 weeks of age). Stress was induced for five consecutive days (twice daily). At the end of the experiment, following anesthesia with pentobarbital, the rats were decapitated and dissected to remove pancreas tissue to measure the number and area of islets. Results: Early-life and pubertal stresses alone did not change the number or area of islets. Compared to other interventions, early-life psychological-stress could considerably change the number or area of pancreatic islets. Conclusion: Early life stress predisposes the organism to morphological changes in endocrine pancreas as an increase in Langerhans islets number or area in exposure to stress later in life

Effects of Memantine, an NMDA Antagonist, on Metabolic Syndromes in Female NMRI Mice

Introduction: The brain glutamate neurotransmitter system and its NMDA receptors in the nucleus accumbens play an important role in the incidence of the phenomena of sensitivity and addiction. The present study examined the inhibitory effect of glutamate NMDA receptors in the nucleus accumbens in response to chronic stress. Methods: After the unilateral and bilateral cannula placement in the nucleus accumbens, one group of the animals received different intra-accumbens doses of memantine (0.1, 0.5 and 1 µg/mouse) 5 minutes before receiving the electric shock stress at their soles (using a Communication Box) and the other group received intraperitoneal doses of memantine (0.1, 0.5 and 1mg/kg) 30 minutes before receiving the same shock. Chronic stress increased the animals' plasma corticosterone, food and water intake and weight and reduced their defecation rates and eating latency.  Results: The intraperitoneal administration of memantine increased plasma corticosterone, water intake, fecal weight and eating latency, but had no effect on food intake or weight. The dose and site-dependent intra-accumbens administration of memantine either exacerbated the effects of stress on plasma corticosterone levels and water and food intake, or else had no effect on these parameters. Furthermore, the administration of memantine had no effect on animal’s weight and inhibited the effects of stress on fecal weight and eating latency. Discussion: The inhibition of glutamate NMDA receptors in the nucleus accumbens can inhibit and/or exacerbate the dose and site-dependent effects of chronic stress, with gender playing a significant role in producing this effect

Oral Morphine Consumption Reduces Lens Development in Rat Embryos

Introduction: Consumption of morphine, during pregnancy, in addition to inducing defects in the mother’s nervous system function, caused defects or delays in the formation and evolution of embryonic visual system. In the present study, changes in lens development were assessed in embryos exposed to morphine in utero. Methods: Female Wistar rats (250-300 g) were mated with male rats and pregnancy was determined by sperm observation in vaginal smear. This day was considered as embryonic day zero (E0). The females were then divided randomly into the experimental and the control groups. The control group received tap water and the experimental group received morphine (0.05 mg/ml) in their water. On embryonic day 13 ( E13), blood samples were collected from the retro-orbital sinus of all animals for plasma corticosterone detection. On embryonic day 17(E17), the animals were killed by an overdose of chloroform and the embryos were taken out surgically. The embryos were fixed in 10% formalin for 30 days. At this time, the head of the embryos were removed for tissue processing and Hematoxylin- Eosin (H&E) staining. The samples were evaluated using light microscope and MOTIC software. Results: Our data indicated that plasma corticosterone level was dramatically increased and the lens was thinner in the experimental group. (Although the proliferation of lens cells increased in the experiment group but that lens had delay in removing the proliferated and elongation cells with abnormal density in the lateral part of the lens in comparison with the control group). Moreover, the opening of the eyelids was delayed in the off springs of the mothers who received morphine. Discussion: This study showed that morphine consumption during pregnancy leads to defects in fetal visual system development, particularly in the lens, and eyelids

Effects of Oral Morphine on the Larvae, Pupae and Imago Development in Drosophila Melanogaster

Objective: Previous studies, focusing on the effects of abused drugs, have used miceor rats as the main animal models; the present study tries to introduce a simple animalmodel. For this propose, we investigated the effects of oral morphine consumption byparents on the development of larvae, pupae and imago in Drosophila Melanogaster (D.Melanogaster).Materials and Methods: In this experimental study, twenty male and 20 female D. Melanogasterpupae were housed in test tubes with banana (5 pupae /tube). Male and femalegroups each were divided into three experimental group and one control group, whichwere maintained at 25°C. Morphine (0.2, 0.02, 0.002 mg/ml) was added into the test tubesof the experimental groups. The control group maintained at morphine-free test tube. Themale and female groups with the same treatment were coupled and then female fertilization,egg deposit, larval, pupae and imago stages were studied macro and microscopically.The SPSS software (version 9.01) was used for statistical evaluations.Results: In the experimental groups, in the larvae stage, both increase and decrease oflength and surface area in the pupae stage were observed. The number of larvae pupae,and imago was reduced in the experimental groups.Conclusion: The study showed that oral morphine consumption by parents may affect thedevelopment of larvae, pupation and imago stages in D. Melanogaster. The results alsoshowed that D. Melanogaster may be a reliable anima

Oral Morphine Consumption Reduces Lens Development in Rat Embryos

Objective: Consumption of morphine, during pregnancy, in addition to inducing defects in the mother’s nervous system function, caused defects or delays in the formation and evolution of embryonic visual system. In the present study, changes in lens development was assessed in embryos exposed in utero to morphine. Material and Methods: Female Wistar rats (250-300 g) were mated with male rats and pregnancy was determined by sperm observation in vaginal smear. This day was considered as embryonic day zero (E0). The females were then divided randomly into the experimental and the control groups. The control group received tap water and the experimental group received morphine (0.05 mg/ml) in their water. On embryonic day 13 ( E13), blood samples were collected from the retro-orbital sinus of all animals for plasma corticosterone detection. On embryonic day 17(E17), the animals were killed by an overdose of chloroform and the embryos were taken out surgically. The embryos were fixed in 10% formalin for 30 days. At this time, the head of the embryos were removed for tissue processing and Hematoxylin- Eosin (H&E) staining. The samples were evaluated using light microscope and MOTIC software. Results: Our data indicated that plasma corticosterone level was dramatically increased and the lens was thinner in the experimental group. (Although the proliferation of lens cells increased in the experiment group but that lens had delay in removing the proliferated and elongation cells with abnormal density in the lateral part of the lens in compare with control group.) I have no idea what the authors are stating here. Moreover, the opening of the eyelids was delayed in the off springs of the mothers who received morphine. Conclusions: This study showed that morphine consumption during pregnancy leads to defects in fetal visual system development, particularly in the lens, and eyelids

Influence of Nitric Oxide in the Central Amygdala on the Acquisition and Expression of Morphine-Induced Place Preference in Morphine Sensitized Rats

Effects of intra-central amygdala administration of L-arginine, a nitric oxide precursor, and NG-nitro-L-arginine methyl-ester (L NAME), a nitric oxide synthase inhibitor, on the morphine-induced sensitization and also on the expression of morphine-induced place conditioning in rats were studied. Subcutaneous (s.c.) administration of morphine (2.5, 5 and 7.5 mg/kg) induced place conditioning. Repeated pretreatment of morphine (5 mg/kg, i.p.) followed by 5 days no drug treatment, increased place conditioning induced by morphine (0.5 mg/kg). Repeated intra-central amygdala administration of L-arginine (0.3, 1 and 3 μg/ rat), with morphine during acquisition of sensitization, significantly increased or reduced morphine place conditioning in sensitized rats. The drug administration before testing also increased and reduced the expression of morphine place conditioning in sensitized animals. Repeated intra-central amygdala injections of L-NAME (0.3, 1 and 3 μg/rat) with morphine during acquisition of sensitization, reduced the acquisition of morphine place conditioning in the sensitized animals. The drug injection before testing also reduced morphine-induced conditioning. The results indicate that nitric oxide (NO) within the central amygdala may be involved in the acquisition and expression of morphine place conditioning in morphine-sensitized rats