Prevalence of anxiety depression and stress among first year medical students in Tamilnadu.

The present study was to evaluate the examination stress of the first year MBBS students, prior to their university exam by assessing the mood parameters and cortisol level. A cross sectional study was conducted in 150 students of Indira Medical College, Thiruvallur from January to February 2022. The assessment methods implemented were Self-administered, pre-designed questionnaire of DASS 10 scale scoring 0-40, and salivary cortisol by using quantitative ELISA on relaxed (before exam) and stressed (on day of exam) students with prior consent. Respondent data were analysed using the independent t-test and Odds ratio logistic regression analysis was done for strength of association by using (SPSS) version 26.0 and the level of significance *p≤0.05. The prevalence of stress (43%), anxiety (35%), depression (22%) and level of cortisol (2.61±0.41 and 5.14±0.35) between relaxed and stressed respectively were significantly increased due to examination stress despite any significant change in academic performance. Odds ratio of stress (95% CI 2.153), anxiety (3.038), depression (2.513) and salivary cortisol (2.872) were significantly high in stressed. Female students were found to be more susceptible to stress than male students due to examination (p≤0.001**). This study suggests that the medical education and examination are unavoidable stressor in first year students. This could be prevented by providing stress reduction interventions and orientation programmes which could improve student mental well-being and reduce the psychological distress.

Deterioration of lung function and its association with eosinophil count.

Exposure to lethal dust particles has a negative impact on human's health. This work investigated the association between respiratory symptoms and eosinophil levels between quarry workers and the controls. A total of 75 workers exposed to quarry dust and 45 age, sex, body mass index-matched unexposed controls participated in this study. Results of this study indicated that the quarry dust particles produced inflammatory responses, increasing the mean eosinophil level (7.56 ± 2.94), causing allergic respiratory symptoms such as rhinitis , chest tightness, wheeze, sputum production thus impairing the lung function with decline in FEV1(80.84 ±108.8) level in workers exposed to quarry dust compared to controls (P≤0.00**) Conclusion: The presence of increased levels of respiratory irritants in quarry sites may explain the higher prevalence of respiratory infections and exacerbated inflammatory reactions found to ascertain the link between increased eosinophil count and the lung impairment in quarry workers.

Protective effect of Triphala on cold stress-induced behavioral and biochemical abnormalities in rats.

Stress is one of the basic factors in the etiology of number of diseases. Cold-stress occurs when the surrounding temperature drops below 18 degrees C, the body may not be able to warm itself, and hence serious cold-related illnesses, permanent tissue damage and death may results. The present study was aimed to investigate the effect of Triphala (Terminalia chebula, Terminalia belerica and Emblica officinalis) against the cold stress-induced alterations in the behavioral and biochemical abnormalities in four different groups (saline control, Triphala, cold-stress and Triphala with cold-stress) of Wistar strain albino rats. In this study cold-stress (8 degrees C for 16 h/d/15 days) was applied and the oxidative stress was assessed by measuring the extent of lipid peroxidation (LPO) and the changes in corticosterone levels. Upon exposure to the cold-stress, a significant (P<0.05) increase in immobilization with decrease in rearing, grooming, and ambulation behavior was seen in open field. Following cold-exposure, significant increase in the LPO and corticosterone levels was observed. Oral administration of Triphala (1 g/kg/animal body weight) for 48 days significantly prevented these cold stress-induced behavioral and biochemical abnormalities in albino rats. The results of this study suggest that Triphala supplementation can be regarded as a protective drug against stress.

Efficacy of DL-alpha-lipoic acid on methanol induced free radical changes, protein oxidative damages and hsp70 expression in folate deficient rat nervous tissue.

DL-alpha-Lipoic acid (LPA) was reported to be effective in reducing free radicals generated by oxidative stress. The protective of effect of LPA on methanol (MeOH) induced free radical changes and oxidative damages in discrete regions of rat brain have been reported in this study. Folate deficient rat (FDD) model was used. The five animal groups (saline control, FDD control, FDD+MeOH, FDD+LPA+MeOH, LPA control) were used. The FDD+MeOH and FDD+LPA+MeOH animals were injected intraperitoneally with methanol (3gm/kg). After 24h, the level of free radical scavengers such as, superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione was estimated in six discrete regions of brain, retina and optic nerve. Level of protein thiol, protein carbonyl and lipid peroxidation was also estimated. Expression of heat shock protein 70 mRNA (hsp70) was studied in the cerebellum and hippocampus by reverse transcriptase PCR. All the samples showed elevation in the level of free radical scavenging enzymes and reduced level of glutathione in the FDD+MeOH group in relation to the other groups. hsp70 expression was more in FDD+MeOH group when compared to FDD+LPA+MeOH group. In conclusion, MeOH exposure leads to increased free radical generation and protein oxidative damages in the rat nervous tissue. Treatment with LPA prevents oxidative damage induced by MeOH exposure.

Hypolipidemic effect of triphala in experimentally induced hypercholesteremic rats.

Hypercholesteremia is one of the risk factors for coronary artery disease. The present study highlights the efficacy of Ayurvedic herbal formulation Triphala (Terminalia chebula, Terminalia belerica, and Emblica officinalis) on total cholesterol, Low density lipoprotein (LDL), Very low density lipoprotein (VLDL), High density lipoprotein (HDL) and free fatty acid in experimentally induced hypercholesteremic rats. Four groups of rats were employed namely control, Triphala treated, hypercholesterolemia rats (4% Cholesterol + 1% cholic acid + egg yolk) and Triphala pre-treatment in hypercholesteremic rats. Results showed significant increase in the total cholesterol, LDL, VLDL, and free fatty acid in hypercholesteremic rats were significantly reduced in Triphala treated hypercholesteremic rats. The data demonstrated that Triphala formulation was associated with hypolipidemic effects on the experimentally induced hypercholesteremic rats.

Effect of methanol-induced oxidative stress on the neuroimmune system of experimental rats.

It is well known that the nervous system has increased susceptibility to methanol intoxication. The present study reveals the effect of methanol intoxication on antioxidant status, lipid peroxidation and DNA integrity in hypothalamic-pituitary-adrenal (HPA) axis organs and spleen. Non-specific and specific immune functions were analyzed. In addition, open field behavior, plasma corticosterone level and blood methanol level were estimated. Male Wistar albino rats were intoxicated with methanol (2.37 g/kg b.wt., i.p.) for 1 day, 15 and 30 days. Administration of methanol showed significant increase in enzymatic (superoxide dismutase, catalase, glutathione peroxidase), non-enzymatic (reduced glutathione and Vitamin C) antioxidants and lipid peroxidation (LPO) in hypothalamus and adrenal gland of day 1 group. However, decrease in enzymatic and non-enzymatic antioxidants with concomitant increase in LPO level were observed in 15 and 30 days groups. Plasma corticosterone level was significantly increased in day 1 and 15 days groups whereas, 30 days methanol intoxication group showed considerable decrease in corticosterone level compared with control animals. Cell-mediated immune response of footpad thickness was significantly decreased with an increased leukocyte migration inhibition. Humoral immune response of antibody titers was elevated in methanol-intoxicated groups. Neutrophil functions, adherence and phagocytic index (PI) were found to be significantly decreases. Furthermore, significant increase in the avidity index and nitro blue tetrozolium reduction was observed in the methanol exposed animals. Day 1 methanol exposed group showed increased PI compared to the control ones. Methanol exposure for 30 days showed an increased DNA fragmentation in the hypothalamus, adrenal glands, and spleen. In conclusion, exposure to methanol-induced oxidative stress disturbs the HPA-axis function altering the level of corticosterone, which lead to varied non-specific and specific immune response in experimental rats.

Effects of chronic noise stress on spatial memory of rats in relation to neuronal dendritic alteration and free radical-imbalance in hippocampus and medial prefrontal cortex.

Spatial memory is coordinated with different brain regions especially hippocampus (HIP) and medial prefrontal cortex (mPFC). Influence of noise stress on working and reference memory error in rats was evaluated by radial eight-arm maze experiment. Changes in the dendritic count were observed in the brain regions such as CA1, CA3 regions of HIP and layers II, III of mPFC. In order to understand the possible mechanism behind noise stress-induced changes, free radical status and acetylcholinesterase (AChE) activity in HIP and mPFC were evaluated. Plasma corticosterone level was also evaluated. Results obtained in this study showed that after noise-stress exposure, 100 dBA/4h per day for 30 days, working and reference memory error increased significantly (P < 0.05) when compared to control animals. Neuronal dendritic count in the HIP was reduced in the 2nd and 3rd order dendrites but not in the mPFC. Superoxide dismutase, lipid peroxidation, plasma corticosterone level and AChE activity were significantly increased in the 1 day, 15 days and 30 days stress groups animal significantly. Catalase and glutathione peroxidase activity were increased in the 1 day and 15 days noise-stress groups but decreased in the 30 days noise-stress group and GSH level was decreased in all the stress exposed animals. In conclusion, oxidative stress, increased AChE activity, reduced dendritic count in HIP, mPFC regions and elevated plasma corticosterone level which develops in long-term noise-stress exposed rats, might have caused the impairment of spatial memory.

Detoxification of formate by formate dehydrogenase-loaded erythrocytes and carbicarb in folate-deficient methanol-intoxicated rats.

BACKGROUND: Formic acid is a toxic metabolite responsible for the metabolic acidosis in methanol poisoning. Formate dehydrogenase (EC 1.2.1.2) converts formate into CO2 in the presence of NAD. We examined the in vitro and in vivo efficiency of formate dehydrogenase-loaded carrier erythrocytes along with carbicarb in eliminating the formate in methanol-intoxicated folate-deficient rats. METHOD: Formate dehydrogenase-loaded erythrocytes were prepared by hypotonic dialysis method. Carbicarb (carb) (equimolar solution of sodium carbonate and sodium bicarbonate) was used to treat metabolic acidosis. Folate depletion was induced by methotrexate (MTX) treatment. Experimental design consisted of 8 groups: saline control, methanol control, MTX control, ELE control, MTX-methanol control, MTX-methanol-carb, MTX-methanol-carb-ELE, and MTX-MeOH-ELE group. Male Wistar rats treated with MTX (0.3 mg/kg) for a week were injected (i.p.) with methanol (4 g/kg). Twelve hours later, the carbicarb solution was infused, and then a formate dehydrogenase-loaded erythrocytes suspension (40% hematocrit) was infused (i.v.) in bolus. Blood samples were collected every hour for 4 h from the cannulated left jugular vein. Blood methanol and formate were estimated respectively with HPLC and fluorimetric assay. Blood pH, blood pO2, pCO2 and bicarbonate were also measured. RESULTS: There was marked elimination of formate in selected groups. CONCLUSION: Formate dehydrogenase-loaded erythrocytes, along with carbicarb, facilitates removal of formate, in methanol poisoning.

Methanol-induced oxidative stress in rat lymphoid organs.

Methanol is primarily metabolized by oxidation to formaldehyde and then to formate. These processes are accompanied by formation of superoxide anion and hydrogen peroxide. This paper reports data on the effect of methanol on antioxidant status and lipid peroxidation in lymphoid organs such as the spleen, thymus, lymph nodes and bone marrow of rats. Male Wistar albino rats were intoxicated with methanol (2.37 g/kg b.w intraperitoneally) for detecting toxicity levels for one day, 15 d and 30 d, respectively. Administration of methanol at 15 and 30 d significantly (p<0.05) increased lipid peroxidation and decreased the enzymatic (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymatic antioxidants (reduced glutathione and vitamin C) in lymphoid organs. However, lipid peroxidation and enzymatic and non-enzymatic antioxidants in the acute methanol exposed group animals were found to be significantly (p<0.05) increased. In one day methanol intoxication, the levels of free radicals initially increased, and to remove these free radicals, antioxidants levels were elevated, which generally prevented oxidative cell damage. But in longer periods of intoxication, when the generation of reactive free radicals overwhelmed the antioxidant defense, lipid peroxidation increased. Further, decreased antioxidants in 15 and 30 d methanol intoxication may have been due to overutilization of non-enzymatic and enzymatic antioxidants to scavenge the products of lipid peroxidation. In addition, the liver and kidney markers of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea and creatinine significantly increased. This study concludes that exposure to methanol causes oxidative stress by altering the oxidant/antioxidant balance in lymphoid organs of the rat.

Protective effect of Acorus calamus LINN on free radical scavengers and lipid peroxidation in discrete regions of brain against noise stress exposed rat.

Exposure to continuous loud noise is a serious health problem due to excess production of oxygen free radicals. In medical research, more attention is paid to the antioxidant properties of medicinal plants to minimize the harmful effects of radicals. The aim of this study was to evaluate the protective effect of both ethyl acetate and methanolic extract of Acorus calamus LINN against noise stress (30 d, 100 dBA/4h/d) induced changes in the rat brain. We measured the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and the levels of reduced glutathione (GSH), vitamin C, vitamin E, protein thiols and lipid peroxidation (LPO) for the evaluation of oxidative stress status in discrete regions of the rat brain like cerebral cortex, cerebellum, pons-medulla, midbrain, hippocampus and hypothalamus. The results indicated that during exposure of noisy environment ROS generation led to increase in corticosterone, LPO and SOD, but decrease in CAT, GPx, GSH, protein thiols, vitamins C and E levels. Both the ethyl acetate and methanolic extract of Acorus calamus protected most of the changes in the rat brain induced by noise-stress.

Antioxidant property of alpha-asarone against noise-stress-induced changes in different regions of rat brain.

Free radicals and other reactive species are considered to be an important causative factor in the development of neurodegenerative diseases. Recent reports have indicated that exposure to loud noise generates excess oxygen free radicals (OFR) in the brain. Antioxidant properties of medicinal plants are attracting more and more research in medicine, to counteract OFR and to minimize the neurodegenerative processes. The drug alpha-asarone (3, 6 and 9 mg kg(-1) body weight, i.p., for 30 days), one of the active principle components of Acorus calamus Linn., was administered intraperitoneally 1/2 h before the animals were exposed to noise-stress (100 dB for 4 h d(-1), for 30 days). We investigated whether 30 days exposure of noise can produce an oxidative stress. Further, if yes then, could alpha-asarone counteract the stress. This was verified by measuring the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), levels of reduced glutathione (GSH), Vitamin C, Vitamin E, protein thiols and lipid peroxidation (LPO) in different regions of the rat brain. All the three doses of alpha-asarone had an effectively protective role by normalizing the increased SOD and LPO, decreased CAT, GPx, GSH, Vitamins C and E and protein thiols due to noise exposure. Thus, action of alpha-asarone against noise-stress may be due its antioxidant property. Our data proved that antioxidant property of alpha-asarone against noise-stress induced changes in the rat brain. Further, more clinical studies are required to investigate effectiveness of the alpha-asarone in noisy environment in human subjects.