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Insulin is known to increase brain nitric oxide (NO) level and to cause oxidative stress but the relationship between these phenomena has not been well elucidated. This study aimed to examine the role of NO in the insulin-NO-oxidative stress axis in the brain. Mice were grouped into four (n = 5) and treated for seven days with 0.2 ml deionized water (control); 10 I.U./kg insulin; 10 I.U./kg insulin + 50 mg/kg L-NAME; and 50 mg/kg L-NAME. The mice were anaesthesized using ketamine + xylazine and sacrificed at the end of the study. Forebrain was immediately harvested from which brain homogenates were prepared in order to determine NO and malondialdehyde (MDA) concentrations as well as glutathione peroxidase (GPx) activity using commercially available kits. Data were processed using IBM SPSS Statistics 20.0. Nitric oxide values were higher in the insulin group (p 0.05) but not in the insulin+L-NAME (p 0.05) group when compared with the control. Values of MDA in the insulin and insulin+L-NAME groups were higher (p 0.05) and the same (p 0.05), respectively, than those in the control group. The activity of GPx in the insulin group was lower (p 0.05) than, but that of the insulin+L-NAME was the same (p 0.05) as in the control group. Insulin increased NO concentration and oxidative stress as indicated by increased MDA concentration and decreased GPx activity in the treated mice. This insulin effect was reversed by L-NAME (a non-specific NO inhibitor). These data suggest that insulin increased oxidative stress in the brain through an NO-dependent process. Insulin treatment may be harmful to the brain.

Insulin increases brain nitric oxide (NO) level but the mechanism and the significance of the effect on memory are not fully understood. This study aimed to demonstrate the mechanism of insulin-induced increase in oxidative stress (OS) and its consequences on learning and memory. Twenty four mice were assigned to groups (n = 6) and treated daily for seven days with water (control), insulin, insulin+Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME) and L-NAME, respectively. Memory was assessed using Y-maze; NO, malondialdehyde (MDA) and glutathione peroxidase (GPx) in brain homogenate were also determined. There was no difference between the groups in the number of entries into the arms and time spent in them, and in number of and percentage alternations performed by the mice, indicating normal memory function of the control and treated mice. NO level in the insulin group was higher compared to the control (p = .018), while those of the other groups were statistically the same compared to the control group. MDA values in the insulin group were higher (p = .001) than those of the control, while those of the other groups were statistically the same compared to those of the control group. GPx activity in the insulin group was lower compared to control (p = .004), while that of the other groups was not significantly different compared to control. It was concluded that insulin treatment increased brain level of NO and OS through increased malondialdehyde level and glutathione peroxidase activity; insulin treatment did not affect long-term visuo-spatial and short-term working memory in the animals. Insulin treatment may have deleterious effects on the brain through increased NO and OS levels.

The effects of Vitamins C & E on Aspirin - induced gastric mucosal damage on gastric ulcer parameters and stomach oxidative stress markers were determined in acute and sub-acute studies in Wistar rats. Aspirin produced a significant (p

Insulin is a common hypoglycaemic agent used to treat diabetes, but it has also been reported to exert other effects on the body including modulation cognition. Reported findings on insulin effect on learning and memory are scanty and often conflicting. This study was aimed at evaluating the effect of sub-acute insulin therapy on visio-spatial learning and memory using Barnes maze. Twelve young mice of both sexes, weighing between 20 – 22 g, were divided into control and insulin-treated groups (n = 6). They were administered subcutaneously with deionized water (control) or insulin (10 I.U./kg/day) for seven days. During the last three days of treatments, the mice were subjected to two-day training and one-day probe trial of Barnes maze. Number of primary head searches on day 2 was reduced compared to day 1 for both the insulin-treated (4.17 ± 0.8 s and 11.45 ± 1.9 s) and control (10.0 ± 3.2 s and 19.95 ± 4.5 s) groups (P < 0.05), but the values obtained in the two groups did not differ (P > 0.05). Similarly, there was no difference between the insulin-treated and control groups in latency to locate the escape hole, time spent and number of head searches per quadrant. It was concluded that sub-acute insulin therapy did not affect long-term visio-spatial learning and memory in mice.Keywords: insulin, visio-spatial learning and memory, long-term memory, Barnes maze, mice