Alterations in glutathione, nitric oxide and 3‑nitrotyrosine levels following exercise and/or hyperbaric oxygen treatment in mice with diet‑induced diabetes

Abstract

Oxidative stress is involved in the development of diabetes. Nitric oxide (NO) contributes to oxidative stress, affects the synthesis of glutathione (GSH) in tissues and also regulates important physiological processes. The levels of nitrosative stress, assessed by measuring the levels of 3-nitrotirosina (3NT) as well as the bioavailability of NO are modulated by exercise and hyperbaric oxygenation (HBO). The aim of the present study was to evaluate the effects of exercise and HBO on the levels of NO, 3NT and GSH in tissues of various organs obtained from diabetic mice. Female mice were fed a high-fat/high-fructose diet to induce diabetes. Mice with diabetes were subjected to exercise and/or HBO. Initial and final concentrations of NO, 3NT and GSH were assessed in the muscle, liver, kidney, heart, spleen, lung, brain, visceral adipose, thoracic aorta and small intestine. Diabetes did not affect initial values of NO, although it significantly increased the levels of 3NT. The basal level of GSH in the diabetic group was lower than or comparable to that of the control group in the majority of the organs assessed. A negative correlation was observed between 3NT and GSH levels in the initial values of all tissues of the control group only, whereas all pathological tissues showed a positive correlation between NO and GSH. There was an increase or a stabilization of GSH levels in the majority of the organs in all treated mice despite the increase in nitrosative stress.

Reduced Liver Autophagy in High-Fat Diet Induced Liver Steatosis in New Zealand Obese Mice

“…We were able to show an accumulation of protein-bound 3-nitrotyrosine and 4-HNE modified proteins in the high-fat fed mice. This was also observed in B6 mice on a HFD by Gutiérrez-Camacho et al [ 35 ], although additional challenges were applied in the study. Both protein modifications have been previously shown in HFD-induced stress [ 36 , 37 ] and aging [ 14 , 38 , 39 ].…”

Exercise alleviates diabetic complications by inhibiting oxidative stress-mediated signaling cascade and mitochondrial metabolic stress in GK diabetic rat tissues

“…Excessive ROS production is known to suppress antioxidant defense systems and physical exercise training has been shown to upregulate antioxidant defense mechanisms in several tissues and metabolic disorders ( Golbidi et al, 2012 ; Lima et al, 2015 ). Glutathione, an abundant endogenous antioxidant has been reported to be decreased in type 2 diabetic patients ( Sekhar et al, 2011 ; Lagman et al, 2015 ; Gutiérrez-Camacho et al, 2020 ). In our study, we observed a decrease in the GSH pool in the GK rat tissues, which increased significantly with exercise.…”

Metabolic programming in offspring of mice fed fructose during pregnancy and lactation

“…Furthermore, excessive NO production can disturb the physiological balance between the generation of peroxynitrite, antioxidant defense mechanisms, and signaling pathways involving NO in different tissues. 50 In this study, a high fructose consumption caused an oxidative state in the offspring's liver, demonstrated by an increase in NO and a low content of sulfhydryl. Although these changes (NO and SH) were more present at the dose of 10%/l of fructose, we can take into account that both doses caused DNA damage and that despite this difference was not statistically significant at both doses in relation to the control group, we observed that, regardless of the dose, fructose can cause this imbalance in the offspring.…”

“…The same results were observed by Vitaglione et al, 49 in which an imbalance in oxidative stress affected the transcription of numerous biochemical mediators, which led to of modulation the tissue and cellular events, such as apoptosis, necrosis and fibrosis, which in turn are present in different types of liver diseases. A study by Gutiérrez-Camacho et al 50 using diet-induced diabetes showed an increase in NO content and elevated levels of nitrosative stress, suggesting that any increased elimination of NO by superoxide is offset by an increase in its production in this animal model. Furthermore, excessive NO production can disturb the physiological balance between the generation of peroxynitrite, antioxidant defense mechanisms, and signaling pathways involving NO in different tissues.…”