Age-Related Elevation of Lipid Peroxidation Products: Diminution of Superoxide Dismutase Activity in the Central Nervous System of Rats

Gupta, Ankush; Hasan, Mahdi; Chander, Ramesh; Kapoor, N. K.

doi:10.1159/000213277

Cited by 73 publications

(36 citation statements)

References 9 publications

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“…A growing body of evidence suggests that reactive ROS play a crucial role in the development of these impairments as discussed above (Yamada et al 1995;Kucukatay et al 2007). The increased production of oxidants altered neurotransmitter release and increased membrane permeability (Gupta et al 1991). Besides, free radicals may degrade nitric oxide (NO), which plays an important role as a diffusible intercellular signaling molecule (a neurotransmitter in the central nervous system) (Geyer et al 1997).…”

Section: Resultsmentioning

confidence: 99%

Neurobehavioral changes in mice offspring induced by prenatal exposure to acute toxicity of sodium selenite

2011

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Selenium is an essential element with a narrow margin between beneficial and toxic effects. This study was aimed to determine the neurobehavioral changes resulted from the prenatal exposure of mice to high doses of sodium selenite during fetal and early postnatal development. Atomic absorption for monitoring the placental transfer of selenium to offspring was employed. The developmental observations as well as the behavioral tests, such as sensory motor reflexes, and learning and memory test in automatic reflex conditioner (shuttle box) (active avoidance responses) were applied. Adult mice was assigned into three groups: the first group was remained as a control group given phosphate buffered saline; the second and the third groups were orally administrated sodium selenite at doses of 1 mg/kg and 4 mg/kg of the diet, respectively started from the 7 th day to the end of the gestation period. Appearance of body hair and opening of eyes of the pups from treated mothers were delayed in a dose-dependent manner. The body weight gain came significantly lower than those of the control especially at the higher dose. Selenite also inhibited the sensory motor reflexes in all elements of acts and postures in a dose dependent manner. The active avoidance training-test indicated that selenite exposure was associated with learning impairment. Acetylcholine recorded a significant decrease in almost all the period of this study. By using atomic absorption, we found a significant high concentration of selenium in the brain, liver and kidney until the 40 th postnatal day, indicating active transfer of selenium from mothers to embryos.

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Section: Resultsmentioning

confidence: 99%

Neurobehavioral changes in mice offspring induced by prenatal exposure to acute toxicity of sodium selenite

2011

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“…It has also been reported that oxidative stress may in part contribute to the pathogenesis of PH in a MCT model [33,34] . The antioxidative defense is largely provided by several enzymes such as SOD, GSH-Px, and CAT [35][36][37] . Meng and coworkers [25] indicated that low doses of SO 2 (22 and 56 mg/m 3 ) caused significant increases in SOD, GSH-Px, and CAT activities in the lungs.…”

Section: Discussionmentioning

confidence: 99%

Effects of endogenous sulfur dioxide on monocrotaline-induced pulmonary hypertension in rats¹

Jin

Zhao

et al. 2008

Acta Pharmacologica Sinica

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Aim: The present study aimed to explore the protective effect of endogenous sulfur dioxide (SO 2 ) in the development of monocrotaline (MCT)-induced pulmonary hypertension (PH) in rats. Methods: Forty Wistar rats were randomly divided into the MCT group receiving MCT treatment, the MCT+L-aspartate-β-hydroxamate (HDX) group receiving MCT plus HDX treatment, the MCT+SO 2 group receiving MCT plus SO 2 donor treatment, and the control group. Mean pulmonary artery pressure (mPAP) and structural changes in pulmonary arteries were evaluated. SO 2 content, aspartate aminotransferase activity, and gene expression were measured. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), reduced glutathione (GSH), oxidized glutathione, and malondialdehyde (MDA) levels were assayed. Results: In the MCT-treated rats, mPAP and right ventricle/(left ventricle+septum) increased significantly (P<0.01), pulmonary vascular structural remodeling developed, and SOD, GSHPx, CAT, GSH, and MDA levels of lung homogenates significantly increased (P<0.01) in association with the elevated SO 2 content, aspartate aminotransferase activity, and gene expression, compared with the control rats. In the MCT+HDX-treated rats, lung tissues and plasma SO 2 content and aspartate aminotransferase activities decreased significantly, whereas the mPAP and pulmonary vascular structural remodeling were markedly aggravated with the decreased SOD, CAT, and GSH levels of lung tissue homogenates compared with the MCTtreated rats (P<0.01). In contrast, with the use of a SO 2 donor, the pulmonary vascular structural remodeling was obviously lessened with elevated lung tissue SOD, GSH-Px, and MDA content, and plasma SOD, GSH-Px, and CAT levels. Conclusion: Endogenous SO 2 might play a protective role in the pathogenesis of MCT-induced PH and promote endogenous antioxidative capacities.

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“…Levels of lipidperoxidation products are also increased with aging (44,83,87,97,108,113,119,123). In addition, aging-related oxidative modification of different proteins causes changes in protein structure, enzyme activities, transcriptional activities, and signal-transduction pathways (32,70,103,111,112,124), leading to age-related diseases.…”

Section: Liu and Xumentioning

confidence: 99%

p53, Oxidative Stress, and Aging

Liu

Xu²

2011

Antioxidants & Redox Signaling

281

198

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Mammalian aging is associated with elevated levels of oxidative damage of DNA, proteins, and lipids as a result of unbalanced prooxidant and antioxidant activities. Accumulating evidence indicates that oxidative stress is a major physiological inducer of aging. p53, the guardian of the genome that is important for cellular responses to oxidative stresses, might be a key coordinator of oxidative stress and aging. In response to low levels of oxidative stresses, p53 exhibits antioxidant activities to eliminate oxidative stress and ensure cell survival; in response to high levels of oxidative stresses, p53 exhibits prooxidative activities that further increase the levels of stresses, leading to cell death. p53 accomplishes these context-dependent roles by regulating the expression of a panel of genes involved in cellular responses to oxidative stresses and by modulating other pathways important for oxidative stress responses. The mechanism that switches p53 function from antioxidant to prooxidant remains unclear, but could account for the findings that increased p53 activities have been linked to both accelerated aging and increased life span in mice. Therefore, a balance of p53 antioxidant and prooxidant activities in response to oxidative stresses could be important for longevity by suppressing the accumulation of oxidative stresses and DNA damage. Antioxid. Redox Signal. 15, 1669-1678.p53 Is a Critical Tumor Suppressor

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Age-Related Elevation of Lipid Peroxidation Products: Diminution of Superoxide Dismutase Activity in the Central Nervous System of Rats

Cited by 73 publications

References 9 publications

Neurobehavioral changes in mice offspring induced by prenatal exposure to acute toxicity of sodium selenite

Neurobehavioral changes in mice offspring induced by prenatal exposure to acute toxicity of sodium selenite

Effects of endogenous sulfur dioxide on monocrotaline-induced pulmonary hypertension in rats¹

p53, Oxidative Stress, and Aging

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Age-Related Elevation of Lipid Peroxidation Products: Diminution of Superoxide Dismutase Activity in the Central Nervous System of Rats

Cited by 73 publications

References 9 publications

Neurobehavioral changes in mice offspring induced by prenatal exposure to acute toxicity of sodium selenite

Neurobehavioral changes in mice offspring induced by prenatal exposure to acute toxicity of sodium selenite

Effects of endogenous sulfur dioxide on monocrotaline-induced pulmonary hypertension in rats1

p53, Oxidative Stress, and Aging

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Effects of endogenous sulfur dioxide on monocrotaline-induced pulmonary hypertension in rats¹