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Testis glutathione peroxidase and phospholipid hydroperoxide glutathione peroxidase activities in aminoguanidine-treated diabetic rats 总被引:3,自引:0,他引:3
Severe steroidogenic and spermatogenic alterations are reported in association with diabetic manifestations in humans and experimental animals. This study was planned to determine whether oxidative stress is involved in diabetes-induced alterations in the testes. Diabetes was induced in male rats by injection of 50 mg/kg of streptozotocin (STZ). Ten weeks after injection of STZ, levels of selenium and activities of selenium dependent-glutathione peroxidase (GPx) and phospholipid hydroperoxide glutathione peroxidase (PHGPx) were measured in rat testis. Lipid and protein oxidations were evaluated as measurements of testis malondialdehyde (MDA) and protein carbonyl levels, respectively. Testis sulfydryl (SH) levels were also determined. The control levels of GPx and PHGPx activities were found to be 46.5 +/- 6.2 and 108.8 +/- 19.8 nmol GSH/mg protein/min, respectively. Diabetes caused an increase in testis GPx (65.0 +/- 21.1) and PHGPx (155.9 +/- 43.1) activities but did not affect the levels of selenium or SH. However, the testis MDA and protein carbonyl levels as markers of lipid and protein oxidation, respectively, did not increase in the diabetic group. Aminoguanidine (AG) treatment of diabetic rats returned the testis PHGPx activity (136.5 +/- 24.9) to the control level but did not change the value of GPx activity (69.2 +/- 17.4) compared with diabetic group. MDA and protein carbonyl levels in testis were not affected by AG treatment of diabetic rats, but interestingly AG caused SH levels to increase. The results indicate that reactive oxygen radicals were not involved in possible testicular complications of diabetes because diabetes-induced activations of GPx and PHGPx provided protection against oxidative stress, which was reported to be related to some diabetic complications. 相似文献
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Tanrikulu-Kiliç F Bekpinar S Unlüçerçi Y Orhan Y 《Physiological research / Academia Scientiarum Bohemoslovaca》2006,55(3):285-290
This study was performed to test whether plasma homocysteine concentrations are related to insulin resistance in healthy premenopausal women. For this purpose, the relationship between insulin resistance (as assessed by HOMA index) and fasting plasma homocysteine level was determined in 83 healthy volunteers. The results indicated that homocysteine concentrations did not vary as a function of HOMA index (r = -0.147). Plasma homocysteine concentrations also did not vary as a function of other parameters of insulin resistance such as HDL-cholesterol and triglycerides, which they correlated inversely with body mass index (BMI). Furthermore, when individuals were classified according to quartiles of insulin resistance (HOMA index), plasma homocysteine concentrations from the lowest to the highest quartiles were not significantly different. On the other hand, the HOMA index correlated significantly with triglyceride concentrations (r = 0.377, p< 0.001), HDL-cholesterol (r = -0.310, p< 0.01) and BMI (r = 0.468, p< 0.001). These results suggest that plasma homocysteine concentrations are not related to insulin resistance and/or metabolic abnormalities associated with it in premenopausal women. 相似文献
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Seval Develi‐Is Seldag Bekpinar Esra Betul Kalaz Betul Evran Yesim Unlucerci Mine Gulluoglu Mujdat Uysal 《Cell biochemistry and function》2013,31(2):122-128
This study was designed to investigate the role of HO‐1 induction in prevention of thioacetamide (TAA)‐induced oxidative stress, inflammation and liver damage. The changes in hepatic dimethylarginine dimethylaminohydrolase (DDAH) activity as well as plasma arginine and asymmetric dimethylarginine (ADMA) levels were also measured to evaluate nitric oxide (NO) bioavailability. Rats were divided into four groups as control, hemin, TAA and hemin + TAA groups. Hemin (50 mg kg?1, i.p.) was injected to rats 18 h before TAA treatment to induce HO‐1 enzyme expression. Rats were given TAA (300 mg kg?1, i.p.) and killed 24 h after treatment. Although TAA treatment produced severe hepatic injury, upregulation of HO‐1 ameliorated TAA‐induced liver damage up to some extent as evidence by decreased serum alanine transaminase, aspartate transaminase and arginase activities and histopathological findings. Induction of HO‐1 stimulated antioxidant system and decreased lipid peroxidation in TAA‐treated rats. Myeloperoxidase activity and inducible NO synthase protein expression were decreased, whereas DDAH activity was increased by hemin injection in TAA‐treated rats. Induction of HO‐1 was associated with increased arginine levels and decreased ADMA levels, being the main determinants of NO production, in plasma of TAA‐treated rats. In conclusion, our results indicate that HO‐1 induction alleviated increased oxidative stress and inflammatory reactions together with deterioration in NO production in TAA‐induced liver damage in rats. Copyright © 2012 John Wiley & Sons, Ltd. 相似文献
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Sibel ?zyazgan Yesim Unlucerci Selda Bekpinar Ahmet G?khan Akkan 《Experimental diabetes research》2000,1(2):145-153
Aim The effect of 8 weeks′ streptozotocin (STZ)-
induced diabetes and aminoguanidine (AMNG), the
inhibitor of advanced glycosylation reaction, treatment
on arteriolar reactivity to vasoactive substances
was investigated in vitro.
Materials and Methods Studies were performed in
untreated control rats (n = 10), STZ-induced (60 mg/kg
i.v.) diabetic rats (n = 10), AMNG-treated (600 mg/l
given in drinking water throughout 8 weeks) control
rats (n = 10) and AMNG-treated (600 mg/l given in
drinking water, beginning at 72h after STZ and
throughout 8 weeks of diabetes) diabetic rats (n = 10).
Results are expressed as the mean ±s.e. Relaxant
responses are expressed as a percentage (%) relaxation
of noradrenaline-induced tone. Statistical comparisons
were made by one-way analysis of variance
(ANOVA) followed by Tukey–Kramer multiple
comparisons test.
Results 1. The decreased body weights (205 ± 6 g)
and increased blood glucose levels (583 ± 8 mg/dl) of
diabetic rats were partially restored by treatment of
aminoguanidine (253 ± 6 g, p < 0.05 and 480 ± 14 mg/dl, p < 0.001, respectively). 2. Diabetes caused a 71%
deficit in maximal endothelium-dependent relaxation
to acetylcholine for noradrenaline precontracted
aortas (p < 0.001). AMNG treatment prevented the
diabetes-induced impairment in endothelium dependent
relaxation (58 ± 8%) to acetylcholine, maximum
relaxation remaining in the non-diabetic range
(78 ± 4%). 3. Neither diabetes nor treatment affected endothelium-independent relaxation (pD2 and max.
Relax.) to sodium nitroprusside. 4. Vasoconstrictor
responses (pD2 and Max. Contraction) to noradrenaline
and KCl were not influenced by the diabetic
state and treatment.
Conclusion Our data suggest that 8 weeks of
experimental diabetes is associated with a decreased
endothelium-dependent vasodilatation. AMNG
treatment may prevent diabetes-induced endothelial
dysfunction. This may be mediated via the prevention
of advanced glycosylation end product formation,
the enhanced release of vasodilator substances
such as prostacyclin, the increased elasticity of blood
vessels, the antioxidant activity and inhibitor activity
of enzyme aldose-reductase by AMNG. 相似文献
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Y M Unlü?er?i R Bulut S Bekpinar L Kuntsal 《Journal of trace elements in medicine and biology》1999,13(3):170-175
The mucosal protective effect of ebselen was examined in an ethanol-induced rat gastric lesion model. Examination of gastric tissue samples by light microscopy showed that i.g. exposure to 50% ethanol induced gastric injury, which was more prominent in female rats. Ethanol did not effect the gastric acid secretion examined by means of H(+)-K+ATPase, the increment of which might be harmful in the stomach. But ebselen with or without ethanol kept H(+)-K+ATPase below control levels. Gastric alcohol dehydrogenase (ADH) was mainly responsible for oxidation of ethanol in the stomach before it enters the bloodstream. I.g. ethanol exposure inhibited the ADH activity but ebselen eliminated the ethanol-induced inhibition of this enzyme. Therefore, ebselen exhibited a beneficial effect by increasing the gastric ethanol metabolism and by ameliorating the possible tissue toxicity of ethanol. Consistently, we also found that ebselen diminished the blood ethanol level. A gender difference in the blood ethanol levels existed following the same dose of ethanol but there was no difference in ADH activity. Histologically, mucosal injury following ebselen exposure together with ethanol was less severe compared with ethanol treatment alone. We concluded that the decrease in ethanol-induced mucosal injury following ebselen may have contributed to the inhibition of H(+)-K+ATPase and the activation of ADH by ebselen. 相似文献
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