The Experts below are selected from a list of 36 Experts worldwide ranked by ideXlab platform
Ramazan H Yilmaz - One of the best experts on this subject based on the ideXlab platform.
-
protective role of erdosteine on vancomycin induced oxidative stress in rat liver
Molecular and Cellular Biochemistry, 2006Co-Authors: Mehmet Sahin, Efkan Uz, Seref Olgar, Sevket Ercan Tunc, Cagatay Arslan, Ramazan H YilmazAbstract:Drug-induced liver toxicity is a common cause of liver injury. This study was designed to elucidate whether high dose vancomycin (VCM) induces oxidative stress in liver and to investigate the protective effects of erdosteine, an Expectorant Agent. Twenty-two young Wistar rats were divided into three groups as follows: control group, VCM, and VCM plus erdosteine. VCM was administered intraperitoneally in the dosage of 200 mg/kg twice daily for 7 days. Erdosteine was administered orally administered once a day at a dose of 10 mg/kg body weight. The activities of antioxidant enzymes such as superoxide dismutase and catalase as well as the concentration of malondialdehyde, as an indicator of lipid peroxidation, were measured to evaluate oxidative stress in homogenates of the liver. VCM administration increased malondialdehyde levels (p < 0.001), superoxide dismutase (p < 0.01) and catalase (p < 0.001) activities. Erdosteine co-administration with VCM injections caused significantly decreased malondialdehyde levels (p < 0.001), superoxide dismutase (p < 0.01) and catalase (p < 0.001) activities in liver tissue when compared with VCM alone. It can be concluded that erdosteine may prevent VCM-induced oxidative changes in liver by reducing reactive oxygen species.
-
in vivo evidences suggesting the role of oxidative stress in pathogenesis of vancomycin induced nephrotoxicity protection by erdosteine
Toxicology, 2005Co-Authors: Faruk Oktem, Ramazan H Yilmaz, Meltem Koyuncu Arslan, Fehmi Ozguner, Ozden Candir, Metin Ciris, Efkan UzAbstract:Abstract The aims of this study were to examine vancomycin (VCM)-induced oxidative stress that promotes production of reactive oxygen species (ROS) and to investigate the role of erdosteine, an Expectorant Agent, which has also antioxidant properties, on kidney tissue against the possible VCM-induced renal impairment in rats. Rats were divided into three groups: sham, VCM and VCM plus erdosteine. VCM was administrated intraperitoneally (i.p.) with 200 mg kg −1 twice daily for 7 days. Erdosteine was administered orally. VCM administration to control rats significantly increased renal malondialdehyde (MDA) and urinary N -acetyl-β- d -glucosaminidase (NAG, a marker of renal tubular injury) excretion but decreased superoxide dismutase (SOD) and catalase (CAT) activities. Erdosteine administration with VCM injections caused significantly decreased renal MDA and urinary NAG excretion, and increased SOD activity, but not CAT activity in renal tissue when compared with VCM alone. Erdosteine showed histopathological protection against VCM-induced nephrotoxicity. There were a significant dilatation of tubular lumens, extensive epithelial cell vacuolization, atrophy, desquamation, and necrosis in VCM-treated rats more than those of the control and the erdosteine groups. Erdosteine caused a marked reduction in the extent of tubular damage. It is concluded that oxidative tubular damage plays an important role in the VCM-induced nephrotoxicity and the modulation of oxidative stress with erdosteine reduces the VCM-induced kidney damage both at the biochemical and histological levels.
-
the effects of erdosteine on the activities of some metabolic enzymes during cisplatin induced nephrotoxicity in rats
Pharmacological Research, 2004Co-Authors: Ramazan H Yilmaz, Sadik Sogut, Mustafa Iraz, Zeki Yildirim, Omer Akyol, Huseyin Ozyurt, Serdar GergerliogluAbstract:Abstract Cisplatin is one of the widely used chemothrapeutic Agents. One of the major side effects of the drug is renal toxicity. The aims of the presented study was (1) to investigate the effect of cisplatin on some renal metabolic enzyme activities such as hexokinase (HK), glucose-6-phosphate dehydrogenase (G6PD), lactate dehydrogenase (LDH), and malate dehydrogenase (MDH) in an experimental model of acute renal failure and (2) to examine the protective role of erdosteine, an Expectorant Agent which has also antioxidant properties on cisplatin–induced nephrotoxicity and the enzyme activities mentioned above. Female Wistar albino rats were divided into three groups: sham operation group (n=6), cisplatin group (n=9), erdostein+cisplatin group (n=8). All the chemicals used were applied intraperitoneally. Hexokinase, G6PD, LDH, and MDH activities were determined in the kidney supernatant at the end of the surgical procedures. Spectrophotometric methods were used to determine the activities of above-mentioned enzymes in the kidney tissue. Hexokinase and G6PD activities were found to be increased in cisplatin group compared to control group. G6PD activities were found to be decreased in erdosteine+cisplatin group compared to cisplatin group. There were minimal changes in LDH and MDH activities of the two study groups compared with the control group. The results obtained suggested that the glucose metabolizing metabolic pathways of renal tissue were partially affected from cisplatin toxicity and erdosteine have some protective effects on these enzyme activities.
Efkan Uz - One of the best experts on this subject based on the ideXlab platform.
-
protective role of erdosteine on vancomycin induced oxidative stress in rat liver
Molecular and Cellular Biochemistry, 2006Co-Authors: Mehmet Sahin, Efkan Uz, Seref Olgar, Sevket Ercan Tunc, Cagatay Arslan, Ramazan H YilmazAbstract:Drug-induced liver toxicity is a common cause of liver injury. This study was designed to elucidate whether high dose vancomycin (VCM) induces oxidative stress in liver and to investigate the protective effects of erdosteine, an Expectorant Agent. Twenty-two young Wistar rats were divided into three groups as follows: control group, VCM, and VCM plus erdosteine. VCM was administered intraperitoneally in the dosage of 200 mg/kg twice daily for 7 days. Erdosteine was administered orally administered once a day at a dose of 10 mg/kg body weight. The activities of antioxidant enzymes such as superoxide dismutase and catalase as well as the concentration of malondialdehyde, as an indicator of lipid peroxidation, were measured to evaluate oxidative stress in homogenates of the liver. VCM administration increased malondialdehyde levels (p < 0.001), superoxide dismutase (p < 0.01) and catalase (p < 0.001) activities. Erdosteine co-administration with VCM injections caused significantly decreased malondialdehyde levels (p < 0.001), superoxide dismutase (p < 0.01) and catalase (p < 0.001) activities in liver tissue when compared with VCM alone. It can be concluded that erdosteine may prevent VCM-induced oxidative changes in liver by reducing reactive oxygen species.
-
in vivo evidences suggesting the role of oxidative stress in pathogenesis of vancomycin induced nephrotoxicity protection by erdosteine
Toxicology, 2005Co-Authors: Faruk Oktem, Ramazan H Yilmaz, Meltem Koyuncu Arslan, Fehmi Ozguner, Ozden Candir, Metin Ciris, Efkan UzAbstract:Abstract The aims of this study were to examine vancomycin (VCM)-induced oxidative stress that promotes production of reactive oxygen species (ROS) and to investigate the role of erdosteine, an Expectorant Agent, which has also antioxidant properties, on kidney tissue against the possible VCM-induced renal impairment in rats. Rats were divided into three groups: sham, VCM and VCM plus erdosteine. VCM was administrated intraperitoneally (i.p.) with 200 mg kg −1 twice daily for 7 days. Erdosteine was administered orally. VCM administration to control rats significantly increased renal malondialdehyde (MDA) and urinary N -acetyl-β- d -glucosaminidase (NAG, a marker of renal tubular injury) excretion but decreased superoxide dismutase (SOD) and catalase (CAT) activities. Erdosteine administration with VCM injections caused significantly decreased renal MDA and urinary NAG excretion, and increased SOD activity, but not CAT activity in renal tissue when compared with VCM alone. Erdosteine showed histopathological protection against VCM-induced nephrotoxicity. There were a significant dilatation of tubular lumens, extensive epithelial cell vacuolization, atrophy, desquamation, and necrosis in VCM-treated rats more than those of the control and the erdosteine groups. Erdosteine caused a marked reduction in the extent of tubular damage. It is concluded that oxidative tubular damage plays an important role in the VCM-induced nephrotoxicity and the modulation of oxidative stress with erdosteine reduces the VCM-induced kidney damage both at the biochemical and histological levels.
Faruk Oktem - One of the best experts on this subject based on the ideXlab platform.
-
in vivo evidences suggesting the role of oxidative stress in pathogenesis of vancomycin induced nephrotoxicity protection by erdosteine
Toxicology, 2005Co-Authors: Faruk Oktem, Ramazan H Yilmaz, Meltem Koyuncu Arslan, Fehmi Ozguner, Ozden Candir, Metin Ciris, Efkan UzAbstract:Abstract The aims of this study were to examine vancomycin (VCM)-induced oxidative stress that promotes production of reactive oxygen species (ROS) and to investigate the role of erdosteine, an Expectorant Agent, which has also antioxidant properties, on kidney tissue against the possible VCM-induced renal impairment in rats. Rats were divided into three groups: sham, VCM and VCM plus erdosteine. VCM was administrated intraperitoneally (i.p.) with 200 mg kg −1 twice daily for 7 days. Erdosteine was administered orally. VCM administration to control rats significantly increased renal malondialdehyde (MDA) and urinary N -acetyl-β- d -glucosaminidase (NAG, a marker of renal tubular injury) excretion but decreased superoxide dismutase (SOD) and catalase (CAT) activities. Erdosteine administration with VCM injections caused significantly decreased renal MDA and urinary NAG excretion, and increased SOD activity, but not CAT activity in renal tissue when compared with VCM alone. Erdosteine showed histopathological protection against VCM-induced nephrotoxicity. There were a significant dilatation of tubular lumens, extensive epithelial cell vacuolization, atrophy, desquamation, and necrosis in VCM-treated rats more than those of the control and the erdosteine groups. Erdosteine caused a marked reduction in the extent of tubular damage. It is concluded that oxidative tubular damage plays an important role in the VCM-induced nephrotoxicity and the modulation of oxidative stress with erdosteine reduces the VCM-induced kidney damage both at the biochemical and histological levels.
Mehmet Sahin - One of the best experts on this subject based on the ideXlab platform.
-
protective role of erdosteine on vancomycin induced oxidative stress in rat liver
Molecular and Cellular Biochemistry, 2006Co-Authors: Mehmet Sahin, Efkan Uz, Seref Olgar, Sevket Ercan Tunc, Cagatay Arslan, Ramazan H YilmazAbstract:Drug-induced liver toxicity is a common cause of liver injury. This study was designed to elucidate whether high dose vancomycin (VCM) induces oxidative stress in liver and to investigate the protective effects of erdosteine, an Expectorant Agent. Twenty-two young Wistar rats were divided into three groups as follows: control group, VCM, and VCM plus erdosteine. VCM was administered intraperitoneally in the dosage of 200 mg/kg twice daily for 7 days. Erdosteine was administered orally administered once a day at a dose of 10 mg/kg body weight. The activities of antioxidant enzymes such as superoxide dismutase and catalase as well as the concentration of malondialdehyde, as an indicator of lipid peroxidation, were measured to evaluate oxidative stress in homogenates of the liver. VCM administration increased malondialdehyde levels (p < 0.001), superoxide dismutase (p < 0.01) and catalase (p < 0.001) activities. Erdosteine co-administration with VCM injections caused significantly decreased malondialdehyde levels (p < 0.001), superoxide dismutase (p < 0.01) and catalase (p < 0.001) activities in liver tissue when compared with VCM alone. It can be concluded that erdosteine may prevent VCM-induced oxidative changes in liver by reducing reactive oxygen species.
Metin Ciris - One of the best experts on this subject based on the ideXlab platform.
-
in vivo evidences suggesting the role of oxidative stress in pathogenesis of vancomycin induced nephrotoxicity protection by erdosteine
Toxicology, 2005Co-Authors: Faruk Oktem, Ramazan H Yilmaz, Meltem Koyuncu Arslan, Fehmi Ozguner, Ozden Candir, Metin Ciris, Efkan UzAbstract:Abstract The aims of this study were to examine vancomycin (VCM)-induced oxidative stress that promotes production of reactive oxygen species (ROS) and to investigate the role of erdosteine, an Expectorant Agent, which has also antioxidant properties, on kidney tissue against the possible VCM-induced renal impairment in rats. Rats were divided into three groups: sham, VCM and VCM plus erdosteine. VCM was administrated intraperitoneally (i.p.) with 200 mg kg −1 twice daily for 7 days. Erdosteine was administered orally. VCM administration to control rats significantly increased renal malondialdehyde (MDA) and urinary N -acetyl-β- d -glucosaminidase (NAG, a marker of renal tubular injury) excretion but decreased superoxide dismutase (SOD) and catalase (CAT) activities. Erdosteine administration with VCM injections caused significantly decreased renal MDA and urinary NAG excretion, and increased SOD activity, but not CAT activity in renal tissue when compared with VCM alone. Erdosteine showed histopathological protection against VCM-induced nephrotoxicity. There were a significant dilatation of tubular lumens, extensive epithelial cell vacuolization, atrophy, desquamation, and necrosis in VCM-treated rats more than those of the control and the erdosteine groups. Erdosteine caused a marked reduction in the extent of tubular damage. It is concluded that oxidative tubular damage plays an important role in the VCM-induced nephrotoxicity and the modulation of oxidative stress with erdosteine reduces the VCM-induced kidney damage both at the biochemical and histological levels.
