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Mine Inal

Bio: Mine Inal is an academic researcher from Eskişehir Osmangazi University. The author has contributed to research in topics: Glutathione peroxidase & Betaine. The author has an hindex of 18, co-authored 38 publications receiving 1392 citations.

Papers
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TL;DR: Age-related differences in erythrocyte antioxidant enzyme activities are found and peroxidative injury is raised in the aging process, confirming free oxygen radicals have been proposed as important causative agents of aging.

321 citations

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TL;DR: Findings may support that reactive oxygen species increased in malignant cells, and may cause overexpression of antioxidant enzymes and the consumption of coenzyme Q10.

198 citations

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TL;DR: It is demonstrated that the exposure of rats to UVA led to oxidative stress as reflected by increased MDA levels and reduced enzymic antioxidant levels, quercetin may be useful by reducing or preventing photobiologic damage.

149 citations

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TL;DR: Both long-distance and particularly short-distance (100-m) swimming increased the activities of antioxidant defense enzymes, and changes in antioxidant systems due to free radicals were investigated.
Abstract: INAL, M., F. AKYUZ, A. TURGUT, and W. M. GETSFRID. Effect of aerobic and anaerobic metabolism on free radical generation swimmers. Med. Sci. Sports Exerc., Vol. 33, No. 4, 2001, pp. 564–567. Purpose:In this study, changes in antioxidant systems due to free radicals were investigated in short distanc

114 citations

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TL;DR: It is stressed that high concentration of ROS leads to renal ischemia and reperfusion, and quercetin reduces the renal injury by preventing the oxidative stress dependent on ischemIA and reperFusion.
Abstract: Renal ischemia-reperfusion injury occurs in many clinical conditions such as hypovolemic shock, thromboembolism, injury and after renal transplantation. Under these conditions, ROS are considered to be the reason for cellular damage. Bioflavonoids have antioxidant and renoprotective properties. We studied the effect of quercetin, a bioflavonoid, on ischemia and reperfusion in rats. The rats (n = 28) were separated into three groups. Group I was the control group. Animals in groups II (IR) and III (IR + Q) underwent 30 min ischemia and 45 min reperfusion, respectively. Rats, in group III, also received 50 mg kg(-1) quercetin before 45 min of reperfusion. The activities of SOD, CAT, GPx, and concentrations of GSH and GSSGR were determined in renal cortex and erythrocytes. Also, the levels of MDA in renal cortex and plasma, and XO in renal cortex were measured in these groups. The renal cortex XO levels in the IR group were higher than that of the control and IR+Q groups (p<0.001). The renal cortex and plasma MDA levels in the IR group were also found to be higher than the control and IR+Q groups (p<0.01, and p<0.001, respectively). However, a decrease in MAD level of the IR+Q group was found in renal cortex and erythrocytes. In addition, SOD, CAT, and GPx activities in renal cortex and erythrocytes of quercetin-treated animals were enhanced compared to animals of the IR group. Furthermore, there were no significant differences in the SOD, CAT, and GPx activities of the control and IR+Q group. A reduction of GSH and GSSGR levels in IR and IR+Q groups was detected but no significant differences were found between these groups. This study stresses that high concentration of ROS leads to renal ischemia and reperfusion, and quercetin reduces the renal injury by preventing the oxidative stress dependent on ischemia and reperfusion. Quercetin may be used in renal transplantation as an antioxidant drug.

68 citations


Cited by
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Journal ArticleDOI
TL;DR: The finding that a diet rich in antioxidants or the elimination of ROS by antioxidant compounds prevents the development of certain cancers provided the setting for subsequent investigation of the tumorigenic actions of reactive oxygen species.
Abstract: The generation of reactive oxygen radicals in mammalian cells profoundly affects numerous critical cellular functions, and the absence of efficient cellular detoxification mechanisms which remove these radicals can result in several human diseases. Growing evidence suggests that reactive oxygen species (ROS) within cells act as second messengers in intracellular signaling cascades which induce and maintain the oncogenic phenotype of cancer cells. ROS are tumorigenic by virtue of their ability to increase cell proliferation, survival, cellular migration, and also by inducing DNA damage leading to genetic lesions that initiate tumorigenicity and sustain subsequent tumor progression. However, it is also known that ROS can induce cellular senescence and cell death and can therefore function as anti-tumorigenic agents. Therefore, the mechanisms by which cells respond to reactive oxygen species depends on the molecular background of cell and tissues, the location of ROS production and the concentration of individual ROS species. Carcinoma cells produce ROS at elevated rates in vitro, and in vivo many tumors appear persistent to oxidative stress. Thus, the finding that a diet rich in antioxidants or the elimination of ROS by antioxidant compounds prevents the development of certain cancers provided the setting for subsequent investigation of the tumorigenic actions of reactive oxygen species. This review outlines the current knowledge on the various roles of ROS in tumor development and progression.

881 citations

Journal ArticleDOI
Stuart A.S. Craig1
TL;DR: The growing body of evidence shows that betaine is an important nutrient for the prevention of chronic disease and has been shown to protect internal organs, improve vascular risk factors, and enhance performance.

862 citations

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TL;DR: It is suggested that QE treatment has protective effect in diabetes by decreasing oxidative stress and preservation of pancreatic beta-cell integrity.

782 citations

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TL;DR: This work reviews the molecular defects responsible for the malfunctioning of two forms of autophagy - macroautophagy and chaperone-mediated autophage - in old mammals, and highlights general and cell-type specific consequences of dysfunction of the autophagic system with age.
Abstract: A decrease in the turnover of cellular components and the intracellular accumulation of altered macromolecules and organelles are features common to all aged cells. Diminished autophagic activity plays a major role in these age-related manifestations. In this work we review the molecular defects responsible for the malfunctioning of two forms of autophagy, macroautophagy and chaperone-mediated autophagy, in old mammals, and highlight general and cell-type specific consequences of dysfunction of the autophagic system with age. Dietary caloric restriction and antilipolytic agents have been proven to efficiently stimulate autophagy in old rodents. These and other possible experimental restorative efforts are discussed.

757 citations