Changes in antioxidant protein SP-22 of chipmunk carotid bodies during the hibernation season.
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Animals↗
Biomedical subjects
Hiroki Nanri
Publications and source records attributed to Hiroki Nanri.
Hindlimb unloading decreases thioredoxin-related antioxidant proteins and increases thioredoxin-binding protein-2 in rat skeletal muscle.
To investigate role(s) of thioredoxin-related antioxidant proteins in disuse muscle atrophy, we examined the levels of thioredoxin-1 (Trx-1), peroxiredoxin-3/SP-22 (Prx-3) and thioredoxin-binding protein-2 (TBP-2) in rat soleus muscle subjected to hindlimb unloading (HU) for 2, 4, 7 or 14 days. The muscle weight loss was initially observed on day 4. The increases in aclorein- and malondialdehyde-modified proteins, and the decreases in the levels of Trx-1, Prx-3 and Mn-SOD were observed in the late phase of muscle atrophy, whereas, the increase in mRNA expression of TBP-2, a negative regulator of thioredoxin, preceded muscle atrophy. These findings suggest that the decrease of those antioxidant proteins, particularly a marked decrease of Trx-1, may be responsible for the enhanced oxidative damage during the late phase of disuse muscle atrophy. Furthermore, the increase in TBP-2 preceding the muscle atrophy may suppress the thioredoxin-mediated redox signaling, which can be an initial trigger leading to disuse muscle atrophy.
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Blood pressure-lowering effects of lifestyle modification: possible involvement of nitric oxide bioavailability.
Lifestyle modification is recommended as a non-pharmacological approach to treatment of hypertension. Many investigators have reported that exercise has antihypertensive effects, and various mechanisms have been proposed to explain this phenomenon. For example, nitric oxide (NO), which may be increased by exercise, has been reported to play a crucial role in preserving vessel homeostasis both by regulating vascular tone and by exerting anti-atherosclerotic effects. NO is known to be exquisitely sensitive to inactivation by superoxide radicals. However, the relationship between the blood pressure-lowering effect of lifestyle modification and NO bioavailability remains unknown. We investigated the effects of a 12-week lifestyle modification program consisting of mild exercise and diet on changes in blood pressure, plasma nitrate/nitrite (NOx), plasma nitrotyrosine, which is the footprint of NO interaction with reactive oxygen species, and plasma extracellular-superoxide dismutase (EC-SOD). The 12-week lifestyle modification program lowered blood pressure and increased plasma NOx. When the subjects were divided into two groups according to the change of plasma nitrotyrosine as an indicator of NO bioavailability, the subjects whose plasma nitrotyrosine decreased exhibited a significant relationship between the blood pressure-lowering effect of the lifestyle modification and the increase in EC-SOD, whereas those without a decrease in plasma nitrotyrosine exhibited a significant relationship between the blood pressure-lowering effect and the increase in maximum oxygen consumption. These results indicate that the level of NO bioavailability influences the mechanism of the blood pressure-lowering effect of aerobic exercise and diet.
Adult↗
Increase of human MTH1 and decrease of 8-hydroxydeoxyguanosine in leukocyte DNA by acute and chronic exercise in healthy male subjects.
To investigate the effects of exercise on oxidative DNA damage, we measured the levels of 8-hydroxydeoxyguanosine (8-OH-dG, 7,8,dihydro-8-oxo-deoxyguanosine), and mRNA of its sanitization enzyme, human MutT homologue (hMTH1), after mild acute exercise in healthy male subjects. The basal 8-OH-dG levels of physically active subjects were significantly lower than those of sedentary subjects. After mild exercise for 30min, the 8-OH-dG levels of the sedentary subjects significantly decreased. In correspondence with the change of 8-OH-dG levels, the hMTH1 mRNA levels of the physically active subjects were significantly higher than those of the sedentary subjects. The levels of hMTH1 mRNA of sedentary subjects significantly increased after mild exercise. Furthermore, there was a significant negative correlation between the levels of 8-OH-dG and hMTH1 mRNA. These results suggest that a mild exercise has a beneficial effect on the maintenance of low levels of 8-OH-dG probably by keeping the sanitization system at higher levels.
8-Hydroxy-2'-Deoxyguanosine↗
Modulation of the thioredoxin system during inflammatory responses and its effect on heme oxygenase-1 expression.
Heme oxygenase (HO) enzymes catalyze the initial reaction in heme catabolism. HO-1 is an inducible isoform that is up-regulated by diverse stimuli, including inflammatory cytokines and factors that promote oxidative stress. HO-1 is a cytoprotective enzyme that degrades heme, a potent oxidant, to generate carbon monoxide, biliverdin (subsequently reduced to bilirubin), and iron. Recently, we found that thioredoxin (TRX), a disulfide reductase enzyme known to be important for the binding of transcription factors to DNA, contributes to the induction of HO-1 by inflammatory mediators. In the present study, we extended this observation and determined that, similar to HO-1, TRX and TRX reductase (TR) are induced by bacterial lipopolysaccharide in macrophages at the level of mRNA and protein. However, maximal induction of TRX and TR precedes that of HO-1. Increased expression of HO-1 in the cytoplasm of inflammatory cells corresponds to a translocation of TRX into the nucleus of these cells. Finally, transfection of TRX into macrophages promoted an increase in HO-1 protein. Taken together, these data support the concept that the TRX system contributes to the up-regulation of HO-1 under conditions associated with increased oxidative stress.
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Thioredoxin is associated with endotoxin tolerance in mice.
OBJECTIVE: Oxidative stress and subsequent lipid peroxidation appear to be central to the lethal effect of lipopolysaccharide. We hypothesized that induction of an antioxidant protein, thioredoxin, would play an important role in the development of endotoxin tolerance and reduce mortality rates in lipopolysaccharide-treated mice. DESIGN: Prospective, randomized, controlled study. SETTING: University research laboratory. SUBJECTS: Adult, male, ddy mice. INTERVENTIONS: In survival-curve experiments, mice were pre-treated intravenously with a low dose of Escherichia coli lipopolysaccharide (20 microg/mouse, pretreatment group) or saline (control group). A large dose of lipopolysaccharide (200 microg/mouse) subsequently was injected into the tail vein 16 hrs after pretreatment. In experiments to measure the expression of thioredoxin after lipopolysaccharide challenge, mice were injected intravenously with different concentrations of lipopolysaccharide (between 20 and 200 microg/mouse, designated the lipopolysaccharide group) or with saline (control group). MEASUREMENTS AND MAIN RESULTS: The survival rate during the 72-hr observation period was significantly higher in the pretreatment group (82%) than in the control group (30%; p = .025 by Mantel-Cox log rank analysis). After lipopolysaccharide challenge, thioredoxin concentrations in the lung, heart, and liver of mice in the pretreated group were about 1.5- to 2-fold higher than those in the control group. Enhancement in these organs became apparent about 6 hrs after lipopolysaccharide challenge and lasted until at least 24 hrs. The levels of accumulation of 4-hydroxy-2-nonenal modified proteins after a large dose of lipopolysaccharide challenge were lower in the pretreatment group than in the control group. CONCLUSIONS: These results demonstrate that mice with an increased concentration of thioredoxin, induced by pretreatment with a low dose of lipopolysaccharide, had increased survival when given a subsequent high-dose challenge of lipopolysaccharide. Thus, thioredoxin is associated with the development of endotoxin tolerance in mice.
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