Protective effect of taurine against potassium bromate-induced hemoglobin oxidation, oxidative stress, and impairment of antioxidant defense system in blood

2014 ◽  
Vol 31 (3) ◽  
pp. 304-313 ◽  
Author(s):  
Mir Kaisar Ahmad ◽  
Riaz Mahmood
2008 ◽  
pp. 403-411 ◽  
Author(s):  
BI Ognjanović ◽  
SD Marković ◽  
SZ Pavlović ◽  
RV Žikić ◽  
AŠ Štajn ◽  
...  

The effects of selenium (Se) on antioxidant defense system in liver and kidneys of rats with cadmium (Cd)-induced toxicity were examined. Cd exposure (15 mg Cd/kg b.m./day as CdCl2 for 4 weeks) resulted in increased lipid peroxidation (LP) in both organs (p<0.005 and p<0.01). Vitamin C (Vit C) was decreased in the liver (p<0.005), whereas vitamin E (Vit E) was increased in the liver and kidneys (p<0.005 and p<0.05) of Cd-exposed animals. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were decreased in both tissues (p<0.05 and p<0.005), whereas catalase (CAT) activity was decreased only in liver (p<0.005). Glutathione S-transferase (GST) increased in both tissues (p<0.005 and p<0.01). Treatment with Se (0.5 mg Se/kg b.m./day as Na2SeO3 for 4 weeks) significantly increased liver and kidneys SOD and GSH-Px activities (p<0.05 to p<0.005), as well as CAT and GST activities only in the liver (p<0.01). In animals exposed to Se, both the concentrations of Vit C (p<0.01) and Vit E (p<0.005) were increased in both tissues. Co-treatment with Se resulted in reversal of oxidative stress with significant decline in analyzed tissues Cd burden. Our results show that Se may ameliorate Cd-induced oxidative stress by decreasing LP and altering antioxidant defense system in rat liver and kidneys and that Se demonstrates the protective effect from cadmium-induced oxidative damage.


2016 ◽  
Vol 68 (4) ◽  
pp. 877-881 ◽  
Author(s):  
Hong-Bo Li ◽  
Lin Wang ◽  
Zheng-Tao Gu ◽  
Xuan He ◽  
Lei Su

Despite high morbidity and mortality, no effective options are available for the treatment of acute lung injury (ALI). Therefore, the present study investigated the protective effect of honokiol (HK) on ALI via determination of its effect on several key biomarkers. The results of the study showed that HK significantly inhibited the infiltration of neutrophils and protein leakage induced by lipopolysaccharide (LPS) (p<0.05). The pretreatment with HK considerably boosted the endogenous antioxidant defense system to counteract the oxidative stress in LPS-induced ALI by elevating the levels of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH). Moreover, the activity of toxic mediators, such as myeloperoxidase (MPO), and lipid peroxidation were significantly inhibited upon treatment with HK. In order to examine the mechanism of action of HK, its effect was quantified using matrix metalloproteinase-9 (MMP-9) activity in bronchoalveolar lavage fluid (BALF) by gelatin zymography. Pretreatment with HK considerably suppressed the activation of MMP-9 in a concentration-dependent manner. These findings suggest that HK protects from lung injury via inhibition of MMP-9, and by enhancing the activity of the endogenous antioxidant defense system.


2013 ◽  
Vol 304 (5) ◽  
pp. E495-E506 ◽  
Author(s):  
S. Keipert ◽  
M. Ost ◽  
A. Chadt ◽  
A. Voigt ◽  
V. Ayala ◽  
...  

Ectopic expression of uncoupling protein 1 (UCP1) in skeletal muscle (SM) mitochondria increases lifespan considerably in high-fat diet-fed UCP1 Tg mice compared with wild types (WT). To clarify the underlying mechanisms, we investigated substrate metabolism as well as oxidative stress damage and antioxidant defense in SM of low-fat- and high-fat-fed mice. Tg mice showed an increased protein expression of phosphorylated AMP-activated protein kinase, markers of lipid turnover (p-ACC, FAT/CD36), and an increased SM ex vivo fatty acid oxidation. Surprisingly, UCP1 Tg mice showed elevated lipid peroxidative protein modifications with no changes in glycoxidation or direct protein oxidation. This was paralleled by an induction of catalase and superoxide dismutase activity, an increased redox signaling (MAPK signaling pathway), and increased expression of stress-protective heat shock protein 25. We conclude that increased skeletal muscle mitochondrial uncoupling in vivo does not reduce the oxidative stress status in the muscle cell. Moreover, it increases lipid metabolism and reactive lipid-derived carbonyls. This stress induction in turn increases the endogenous antioxidant defense system and redox signaling. Altogether, our data argue for an adaptive role of reactive species as essential signaling molecules for health and longevity.


2009 ◽  
Vol 39 (4) ◽  
pp. 723-730 ◽  
Author(s):  
Jihong Qin ◽  
Qing Liu

In the subalpine zone of the Qinghai–Tibetan Plateau of China, Dragon spruce (Picea asperata Mast.) is commonly used for reforestation. The aim of the present work was to study the effects of seasonally frozen soil on the germination of P. asperata seeds and to investigate whether these effects were associated with resumption of the antioxidant defense system. The nonfrozen treatment resulted in near failure of germination (1%) and was associated with relatively high levels of hydrogen peroxide (H2O2) and low activities of superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxide (APX). Germination of P. asperata seeds at 10 cm under the seasonally frozen soil was higher than that at 5 cm by 26%; this higher germination rate was associated with the recovery of SOD, CAT, and APX activities. The levels of malondialdehyde (MDA) in seeds from seasonally frozen treatments were higher than those in the nonfrozen treatment, implying greater lipid peroxidation and that frozen seeds might have suffered from oxidative stress. The results indicate that seasonally frozen soil facilitated the germination of P. asperata seeds and that germination was closely related to the resumption of antioxidant enzymes activity. Overall, these findings suggest that the disappearance of seasonally frozen ground caused by global warming might result in failure of regeneration of P. asperata.


2014 ◽  
Vol 40 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Khalid Mohammed Naji ◽  
Maher Ali Al-Maqtari ◽  
Adnan Ali Al-Asbahi ◽  
Qais Yusuf M. Abdullah ◽  
R. Nagesh Babu ◽  
...  

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