Biomedical subjects
Publications and source records attributed to G Kaur.
The effect of single dose of NTA on the removal of radio-manganese in various organs and in plasma has been studied in rats which received single i.v. injection of 54Mn(II). The lowered value of radio-manganese in NTA treated rats as compared to control animal indicates that NTA binds rapidly and forms stable and diffusible complex resulting in the fast excretion of the injected 54Mn(II).
The distribution of 54Mn in various organs of pregnant rats and of their 19-day-old fetuses and in non-pregnant female rats of various ages has been studied 18 h after an i.v. injection of 54MnCl2. The results indicate that early neonates are more susceptible to manganese (Mn) than the growing rats. The localization of 54Mn in liver and brain of the embryo was highly significant.
The disappearance and reappearance of iron-59 in plasma and blood at various time intervals has been studied in control, manganese, nickel and tin administered and anaemic rats after a single intravenous injection of an aqueous solution of radioactive iron (III) citrate. Significant difference was observed in the rate of reappearance of iron-59 in the circulation between control and manganese treated animals. The disappearance of iron-59 from the plasma of control and treated animals however did not show any appreciable difference. A significant increase in the radio-iron content was observed in bone marrow, liver and kidney of treated animals as compared to control group forty eight hours after Fe-59.
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Considerable evidence suggests that oxidative stress plays an important role in tissue damage associated with hypoglycemia and other metabolic disorders. The altered brain neurotransmitters metabolism, cerebral electrolyte contents, and impaired blood-brain barrier function may contribute to CNS dysfunction in hypoglycemia. The present study elucidates the effect of starvation and insulin-induced hypoglycemia on the free radical scavanger system--reduced glutathione (GSH) content, glutathione S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GR), gamma-glutamyl transpeptidase (gamma-GTP), gamma-glutamyl cystein synthetase (gamma-GCS), catalase and superoxide dismutase (SOD), and mitochondrial electron transport chain (ETC) complexes I-IV from three different regions of rat brain, namely cerebral hemispheres (CH), cerebellum (CB), and brainstem (BS). Peripheral organs, such as liver and kidney, were also studied. Significant changes in these enzymic activities were observed. The analysis of such alterations is important in ultimately determining the basis of neuronal dysfunction during metabolic stress conditions, such as hypoglycemia, and also defining the nature of these changes may help to develop therapeutic means to cure metabolically stressed tissues.
To address the problem of the pathogenesis in diabetic neuropathy, rats were made diabetic by streptozotocin administration, and discrete brain regions, such as cortex, cerebellum, brainstem, thalamus, and hypothalamus, were sampled for assay of activities of electron transport chain complexes I-IV at 1 and 3 mo after induction of diabetes. Significant decrease was seen in activities of dinitrophenylhydrazine DNPH-coenzyme Q reductase (complex I), coenzyme Q cytochrome-c reductase (complex III), and cytochrome-c oxidase (complex IV) from discrete brain regions with more pronounced changes in complex I. The decline in the complex I, III, and IV activity was more severe in the 3-mo group. Succinate dehydrogenase (SDH) coenzyme Q reductase (complex II), which is an enzyme shared by tricarboxylic acid (TCA) cycle and electron transport chain, showed a significant increase under the same set of conditions. These results suggest that the bioenergetic impairment has an important role in the pathophysiology of diabetes.
The activities of the enzymes related to glutathione synthesis, degradation, and functions as well as reactive oxygen scavenging enzymes were analyzed in different brain regions, such as cerebral hemisphere, cerebellum, brainstem, thalamus, and hypothalamus after 1 and 3 mo of streptozotocin-induced diabetes in rats. Parallel studies were also made in age-matched control rats and insulin-treated diabetic rats. The content of glutathione (GSH) and its synthesizing enzyme gamma-glutamylcystein synthetase and also superoxide dismutase (SOD) and catalase activities (reactive oxygen scavenging enzymes) were significantly decreased from almost all the brain regions studied. However, glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), gamma-glutamyl transpeptidase (gamma-GTP), and glutamine synthetase (GS) activities were increased in the diabetic rat brain. Insulin treatment to the diabetic rats resulted in partial to full recovery in these enzymes activities. The present results emphasize the potentially serious alterations of brain free radical scavenger system in uncontrolled Type I diabetes.
The first study investigated the effect of different doses (0.25, 0.5, 1 g/kg p.o.) of a polyherbal, antiobesity preparation, OB-200G, on the duration of a specific sequence of behaviors (activity, feeding, grooming and resting) associated with the onset of satiety. The recordings were taken at 0, 30 and 60 min, for 10-min periods, immediately after the presentation of sweetened chow to female mice that had been fasted for 16 h. At the end of a 70-min test session, the amount of sweetened chow consumed by each mouse was also recorded. The second study investigated the antagonism of hyperphagia mediated by 2-deoxy-D-glucose (2-DODG), by both OB-200G (0.5 g/kg) and fluoxetine (10 mg/kg). Ingestion of sweetened chow by control mice produced the typical sequence of behaviors associated with the onset of satiety, characterized by initial increase in duration of feeding and active behaviors. With time, these behaviors declined and there was an increase in grooming and resting behaviors. Prefeeding significantly (p < 0.01) decreased the percentage of time spent feeding but also significantly (p < 0.01) increased the duration of active behaviors at 0-10 and 30-40 min. Prefeeding for 20 min advanced the onset and increased the duration of grooming behavior. Treatment with fluoxetine (10 mg/kg) significantly decreased the duration of feeding behavior and increased the active behavior duration at 0-10 and 30-40 min as compared with the control group. There was also a significant (p < 0.01) increase in resting behavior duration with fluoxetine at 60-70 min. OB-200G (0.25-1 g/kg) administration significantly decreased the feeding behavior duration and increased the active-behavior duration at 30-40 min as compared with the control group during that period. However, OB-200G (0.25-I g/kg) did not elicit any significant change in grooming (except decrease at 60-70 min with a 0.5 g/kg dose) and resting behavior duration compared with the control or prefed groups. The amount of sweetened chow consumed significantly decreased (p < 0.01) in 10 and 20 min prefed, fluoxetine-treated and OB-200G-treated (0.5 and 1 g/kg) mice as compared with the control group. Furthermore, the hyperphagia mediated by 2-DODG was significantly antagonized by both OB-200G and fluoxetine. In conclusion, like fluoxetine, OB-200G mediates satiety through operation of normal physiological mechanisms. Antagonism of 2-DODG-hyperphagia by OB-200G and fluoxetine indicates the involvement of a common central pathway (or pathways) in their action.
The present study was carried on adolescents suffering from chronic tonsillitis. Blood (pre and post tonsillectomy) as well as tonsil samples were evaluated for -MDA, SOD and Catalase. Our results showed a decrease in level of MDA and increase in SOD and Catalase levels post tonsillectomy. Presence of MDA and SOD in tonsillar tissue reinforce involvement of oxidative stress in pathophysiology of chronic tonsillitis.
Evidences clearly indicate that HF is accompanied by excessive generation of OFRs and depletion of endogenous antioxidant system. The resultant oxidant stress depresses myocardial contractility and function by decreasing Ca++ uptake in sarcoplasmic reticulum and by impaired Ca(++)-ATPase in cardiac tissue. The various sources of OFRs production in HF include increased production of nitric oxide, cytokines, prostaglandins, auto-oxidation of catecholamines, activation of polymorph leucocytes and ischemia induced xanthine-xanthine oxidase. The prevention of oxidative stress by antioxidant translates into better metabolism and function of myocytes. It appears that antioxidant drugs may represent a novel adjunct to the existing therapeutic armamentarium in patients of HF irrespective of its etiology and severity.
A comparative study on the levels of lipid peroxidation in human platelets has been undertaken in patients of unstable angina and reperfused acute myocardial infarction and matched healthy individuals. Lipid peroxidation increases in these patients, most marked increase were in the patients of reperfused myocardial infarction.