Alterations of Antioxidant Enzyme Expression in Response to Hydrogen Peroxide

Röhrdanz, Elke; Kahl, Regine

doi:10.1016/s0891-5849(97)00159-7

Cited by 169 publications

(92 citation statements)

References 47 publications

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“…However, no other study investigated the differences in cardiac injury markers after renal I/R injury between males and females. The higher level of cardiac CAT in females than in males reported in this study could be explained by the increased activity of SOD which catalyzes the dismutation of O 2 • -into O 2 and H 2 O 2 ; the accumulating H 2 O 2 induces the expression of CAT (Röhrdanz and Kahl 1998). Azevedo et al (2001) reported that CAT level in macrophages was significantly higher in female rats than in males, and ovariectomy led to significant reduction in its level.…”

Section: Discussionmentioning

confidence: 44%

Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

Ibrahim¹,

Elbassuoni²,

Ragy³

et al. 2014

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Abstract. Renal ischemia-reperfusion (I/R) is the major cause of acute renal failure. Renal I/R have distant effects on other organs, especially the heart. The purpose of this study was to investigate cardiac lesion following bilateral renal ischemia (50 minutes) and reperfusion (48 hours) in adult rats, to test sex differences in the development of cardiac lesions after acute renal I/R and to investigate the effect of estrogen on this type of cardiac lesions. 70 adult albino rats were divided into 7 groups: control male, I/R male, control female, I/R female, female with bilateral ovariectomy, I/R female with bilateral ovariectomy and I/R female with bilateral ovariectomy treated with estrogen. Renal and cardiac functions in both sexes were deteriorated following acute renal I/R injury proved by the increase in serum urea, creatinine, lactate dehydrogenase and creatine kinase levels. These cardiac lesions are mainly due to the oxidative stress response in the form of the increase in cardiac tissue lipid peroxide, and the decrease in cardiac tissue glutathione reductase, superoxide dismutase and catalase levels. In conclusion, female rats are more protected from the renal and cardiac lesions following acute renal I/R injury than male, since estrogen significantly decreases these lesions mainly by inhibiting the oxidative stress response.

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Section: Discussionmentioning

confidence: 44%

Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

Ibrahim¹,

Elbassuoni²,

Ragy³

et al. 2014

gpb

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“…Furthermore, the regulation through gene expression of antioxidant defence enzymes, particularly catalase, differs from one cell system to another (Rohrdanz and Kahl, 1998). It has been established that the activities of antioxidant defence enzyme activities in fish vary in different organs of fresh water and marine fish (Wdzieczak et al, 1982;Lemaire et al, 1993), depending upon feeding behaviour (Radi and Markovics, 1988) and other ecological conditions (Winston and Di Giulio, 1991).…”

Section: Discussionmentioning

confidence: 99%

Increased activities of hepatic antioxidant defence enzymes in juvenile gilthead sea bream (Sparus aurata L.) fed dietary oxidised oil: attenuation by dietary vitamin E

et al. 2002

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Previously, we had shown that altering the highly unsaturated fatty acid(HUFA)/vitamin E ratios in sea bream (Sparus aurata) livers significantly affected their peroxidation status, with fish fed the diet rich in HUFA and low in vitamin E showing significantly higher values of lipid peroxidation products, without, however, significant effects on liver antioxidant defence enzyme activities. The aim of the present trial was to further characterise the biochemical indicators of peroxidative stress in juvenile sea bream. A high pro-oxidative stress was induced by feeding diets containing around 7% of the dry weight as n-3HUFA. The potential peroxidative stress was increased by oxidising the oil, increasing the peroxide value of the oil some 10-fold. These oils were fed without or with supplemental vitamin E (α-tocopherol acetate at 200 mg.kg -1 dry diet) giving four diets in total. Fish were sampled after 30 and 60 days of feeding the experimental diets. None of the diets had any serious deleterious effects on growth and mortality of the fish during the trial. Similarly, there were few significant effects due to dietary oxidised oil or supplementary vitamin E on liver lipid and fatty acid profiles of livers and, in particular, the proportions of HUFA were not decreased by dietary oxidised oil. The vitamin E content of the liver reflected the vitamin E contents of the diets but was also affected by dietary oxidised oil being reduced by oxidised oil in fish fed diets without supplemental vitamin E but, unexpectedly, increased by oxidised oil in fish fed diets supplemented with vitamin E. Liver TBARS levels were significantly lower in fish fed diets supplemented with vitamin E whereas dietary oxidised oil had no major effects on lipid peroxidation products. Catalase and superoxide dismutase activities were both increased in fish fed dietary oxidised oil and reduced by supplementary vitamin E after 30 days feeding.In contrast glutathione peroxidase was less affected by the diets, and the activities of glutathione-S-transferase and glutathione reductase were only reduced by dietary vitamin E after 60 days of feeding. However, all the enzyme activities were significantly affected by the duration of feeding, but the number of interactions between the three factors (time, oil and vitamin E) showed that the relationships were complicated. In conclusion, the present study showed that feeding diets containing oxidized oil significantly affected the activities of liver antioxidant defence enzymes and that dietary vitamin E partially abrogated these effects.Growth and survival of the fish were relatively unaffected suggesting that the responses in sea bream offered effective protection. However, the duration of feeding the diets of high pro-oxidative stress was observed to have a hitherto unknown effect, possibly the result of an adaptive process, but which requires further investigation.

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“…Excessive generation of ROS in the CNS has been implicated in neuronal damage resulting from cerebral ischemia and in AD. Oxidant compounds such as H 2 O 2 have been shown to cause perturbation of cell membrane integrity and alteration of mitochondrial function, resulting in an increase in [Ca 2ϩ ]i (43,44). In fact, H 2 O 2 is a naturally occurring oxidant produced by a number of intracellular reactions, and excessive production of this compound is associated with signaling pathways (45) responsible for activating PKC (46), tyrosine kinase (47), and MAPK (45,48).…”

Section: Response To Oxidative Agentsmentioning

confidence: 99%

Phospholipase A2 in the central nervous system

Sun

Xu²,

Jensen

et al. 2004

Journal of Lipid Research

349

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Phospholipase A 2 (PLA 2 ) belongs to a family of enzymes that catalyze the cleavage of fatty acids from the sn-2 position of phospholipids. There are more than 19 different isoforms of PLA 2 in the mammalian system, but recent studies have focused on three major groups, namely, the group IV cytosolic PLA 2 , the group II secretory PLA 2 (sPLA 2 ), and the group VI Ca 2 ؉ -independent PLA 2 . These PLA 2 s are involved in a complex network of signaling pathways that link receptor agonists, oxidative agents, and proinflammatory cytokines to the release of arachidonic acid (AA) and the synthesis of eicosanoids. PLA 2 s acting on membrane phospholipids have been implicated in intracellular membrane trafficking, differentiation, proliferation, and apoptotic processes. All major groups of PLA 2 are present in the central nervous system (CNS). Therefore, this review is focused on PLA 2 and AA release in neural cells, especially in astrocytes and neurons. In addition, because many neurodegenerative diseases are associated with increased oxidative and inflammatory responses, an attempt was made to include studies on PLA 2 in cerebral ischemia, Alzheimer's disease, and neuronal injury due to excitotoxic agents. Information from these studies has provided clear evidence for the important role of PLA 2 in regulating physiological and pathological functions in the CNS. Bazan (1) recognized the important role of arachidonic acid (AA) in the central nervous system (CNS) in the '70s when he observed the rapid and transient release of this fatty acid in the brain due to seizure and cerebral ischemia. The "Bazan effect" has since stimulated over 30 years of investigations attempting to unravel mechanisms regulating AA release from membrane phospholipids in the CNS.Phospholipids in CNS membranes are enriched in polyunsaturated fatty acids (PUFAs) (2). Metabolism of PUFA is stringently controlled by phospholipase A 2 (PLA 2 ) and acyltransferases-known as the "deacylation-reacylation cycle" (3-5). Under normal conditions, free fatty acids (FFAs) released by PLA 2 are rapidly taken up by membrane phospholipids through an energy-dependent process involving CoA and ATP (6). To date, limited information is available on the structure and functions of acyltransferases. However, recent advances in molecular biological techniques have aided in the identification of many genes encoding different groups of PLA 2 and have provided new information on the properties and functions of these molecules.PLA 2 (EC3.1.1.4.) belongs to a family of enzymes that catalyze the cleavage of fatty acids from the sn -2 position of phospholipids. These enzymes are not only important for maintenance of cell membrane phospholipids; they also play a key role in regulating the release of AA, a precursor for synthesis of eicosanoids. In the mammalian system, more than 19 different isoforms of PLA 2 have been identified, and different PLA 2 s have been shown to participate in physiological events related to cell injury, inflammation, and apoptosis (7,8). Re...

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Alterations of Antioxidant Enzyme Expression in Response to Hydrogen Peroxide

Cited by 169 publications

References 47 publications

Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

Increased activities of hepatic antioxidant defence enzymes in juvenile gilthead sea bream (Sparus aurata L.) fed dietary oxidised oil: attenuation by dietary vitamin E

Phospholipase A2 in the central nervous system

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Alterations of Antioxidant Enzyme Expression in Response to Hydrogen Peroxide

Cited by 169 publications

References 47 publications

Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

Increased activities of hepatic antioxidant defence enzymes in juvenile gilthead sea bream (Sparus aurata L.) fed dietary oxidised oil: attenuation by dietary vitamin E

Phospholipase A2 in the central nervous system

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Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats