Age-related change of antioxidant capacities in the cerebral cortex and hippocampus of stroke-prone spontaneously hypertensive rats

Kimoto-Kinoshita, Saori; Nishida, Shozo; Tomura, Takanori

doi:10.1016/s0304-3940(99)00623-0

Cited by 30 publications

(19 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A previous study reported that MnSOD and Cu/ZnSOD are present in the rat brain. 15 The purpose of the present experiment was to examine the effect of the inhibition of the production of superoxide anions in RVLM in a conscious state and whether MnSOD overexpression in the RVLM of SHRSP decreases TBARS levels in the RVLM to the same level as WKY. Inhibition of oxidative stress by MnSOD overexpression in the RVLM of SHRSP decreased MAP, HR, and sympathetic nerve activity, suggesting that an increase in oxidative stress in the RVLM of SHRSP increases MAP via an increase in sympathetic nerve activity in a conscious state.…”

Section: Discussionmentioning

confidence: 99%

“…12,13 Among the target organs of hypertensive vascular diseases, the brain is most affected by aging and oxidative stress. 14,15 The brain contains a high concentration of polyunsaturated fatty acids in its cell membranes. These fatty acids are targets of oxygen-derived free radicals, which cause chain reactions of lipid peroxidation.…”

mentioning

confidence: 99%

“…14 Thiobarbituric acid-reactive substances (TBARS), end products of lipid peroxidation and an indirect marker of oxidative stress, are increased in the brains of SHR compared with those of Wistar-Kyoto rats (WKY). 15 There is no direct evidence, however, of an increase in ROS in the brain in hypertension. Furthermore, the effect of ROS in the brain on sympathetic nerve activity has not been determined in hypertension.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Increased Reactive Oxygen Species in Rostral Ventrolateral Medulla Contribute to Neural Mechanisms of Hypertension in Stroke-Prone Spontaneously Hypertensive Rats

et al. 2004

View full text Add to dashboard Cite

Background-Oxidative stress increases in hypertension. The aim of this study was to determine whether reactive oxygen species (ROS) are increased in the rostral ventrolateral medulla (RVLM) in the brainstem, where the vasomotor center is located, in stroke-prone spontaneously hypertensive rats (SHRSP), and, if so, to determine whether the increased ROS contribute to neural mechanisms of hypertension in SHRSP. Methods and Results-We measured ROS levels in the RVLM of SHRSP and compared them with those in Wistar-Kyoto rats (WKY). Thiobarbituric acid-reactive substances were increased in SHRSP compared with WKY. ROS were measured by electron spin resonance (ESR) spectroscopy. The ESR signal decay rate in the RVLM of SHRSP was significantly increased compared with that in WKY, and this increase was abolished by dimethylthiourea (a hydroxyl radical scavenger). The increased ESR signal decay rate was reduced to the same extent in the presence of desferrioxamine, catalase, and Tiron, indicating that hydroxyl radicals are derived from superoxide anions and hydrogen peroxide. In addition, total superoxide dismutase (SOD) activity in the RVLM was decreased in SHRSP compared with WKY. Furthermore, bilateral microinjection of tempol into the RVLM decreased blood pressure in SHRSP but not in WKY, and MnSOD overexpression in the RVLM of SHRSP decreased blood pressure and inhibited sympathetic nerve activity. Conclusions-These results suggest that superoxide anions in the RVLM, which generate hydroxyl radicals, are increased in SHRSP and contribute to the neural mechanisms of hypertension in SHRSP.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Increased Reactive Oxygen Species in Rostral Ventrolateral Medulla Contribute to Neural Mechanisms of Hypertension in Stroke-Prone Spontaneously Hypertensive Rats

et al. 2004

View full text Add to dashboard Cite

show abstract

“…Accumulation of ROS (63,64) and reduction of antioxidant capacity, DNA repair efficacy and selenoprotein expression (65)(66)(67)(68)(69)(70)(71)(72) have been linked to cellular and organismal aging. However, damage accumulation early in life can also contribute to or accelerate cellular senescence, as DNA breaks and ATM pathway activation are prominent and there are 3-fold more viable clones when SelH shRNA MRC-5 cells are maintained in 3% O 2 than in 20% O 2 incubators (data not shown) as early as two passages after clonal selection.…”

Section: Discussionmentioning

confidence: 99%

Selenoprotein H Suppresses Cellular Senescence through Genome Maintenance and Redox Regulation

Cao

Chen

et al. 2014

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Selenoprotein H (SelH), a proposed redox-responsive DNA-binding protein, is little-studied. Results: SelH shRNA cells display severe proliferation defects and accelerated senescence with abnormal responses to DNA damage and oxidative stress. Conclusion: SelH suppresses senescence and may have important roles in gatekeeping genomic integrity. Significance: Learning how SelH keeps senescence in check is crucial for advancing our understanding linking selenium and aging intervention.

show abstract

“…15, 16 Cell membranes in the brain contain a high concentration of polyunsaturated fatty acids. These fatty acids are targeted by ROS, which elicit chain reactions of lipid peroxidation.…”

Section: Increased Oxidative Stress In the Brain In Hypertensionmentioning

confidence: 99%

Oxidative Stress and Central Cardiovascular Regulation - Pathogenesis of Hypertension and Therapeutic Aspects -

Hirooka

Sagara

Kishi

et al. 2010

Circ J

103

View full text Add to dashboard Cite

Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp ccumulating evidence indicates that the sympathetic nervous system plays an important role in the pathogenesis of hypertension. 1-3 Activation of the sympathetic nervous system is involved in the stages, clinical forms, 24-h blood pressure patterns, end-organ damage, and metabolic abnormalities of hypertension. 1-3 Although peripheral factors are also involved, the central nervous system (CNS) mechanisms are considered crucial. 3-7 The results of recent studies strongly suggest that central sympathetic outflow is increased in hypertension. 3-7 Increased oxidative stress is also involved in the pathogenesis of hypertension. 8 Although there have been many studies regarding target organ damage in hypertension, relatively few studies have addressed the role of oxidative stress in sympathetic nervous system activation. 9-11 Based on the role of angiotensin II (Ang II) in the generation of reactive oxygen species (ROS), the relationship between brain angiotensin and central sympathetic outflow has been examined. 12,13 Our group was the first to report that increased ROS generation in the brainstem contributes to the neural mechanisms of hypertension in hypertensive rats, 14 and we and other investigators have reported additional evidence to support this concept and the potential therapeutic aspects. 9-11 This review focuses on the role of oxidative stress within the brain in the neural pathogenesis of hypertension. Increased Oxidative Stress in the Brain in HypertensionAmong the target organs of hypertensive vascular diseases, the brain is most affected by aging and oxidative stress. 15, 16 Cell membranes in the brain contain a high concentration of polyunsaturated fatty acids. These fatty acids are targeted by ROS, which elicit chain reactions of lipid peroxidation. Oxidative stress is determined by measuring levels of thiobarbituric acid-reactive substances (TBARS), end products of lipid peroxidation. The levels of TBARS reflect those of malondialedehyde, although the assay is not specific for malondialedehyde. 15,17 There are some important points, however, for assessing the levels of TBARS. 17 The medium used for tissue preparation needs to contain a chelating agent and an antioxidant, and conditions for the assay must be kept constant. Therefore, we used another method for assessing the ROS production, which is electron spin resonance (ESR) spectroscopy. The amount of ROS was quantified by monitoring the time-dependent decay of the amplitude of the ESR spectra produced by the nitroxide radical 4-hydroxy-2,2,6,6-tetramethyl-piperidine-N-oxyl (hydroxyl-TEMPO) as a spin probe. 9,14 The signal decay of ESR spectroscopy reflects oxidative stress more directly. Also, it has an advantage for in vivo study. 18 We evaluated oxidative stress in the brains of stroke-prone spontaneously hypertensive rats (SHRSP) compared with normotensive Wistar -Kyoto (WKY) rats. 9, 14 The rostral ventrolateral medulla (RVLM) is the major vaso...

show abstract

Age-related change of antioxidant capacities in the cerebral cortex and hippocampus of stroke-prone spontaneously hypertensive rats

Cited by 30 publications

References 16 publications

Increased Reactive Oxygen Species in Rostral Ventrolateral Medulla Contribute to Neural Mechanisms of Hypertension in Stroke-Prone Spontaneously Hypertensive Rats

Increased Reactive Oxygen Species in Rostral Ventrolateral Medulla Contribute to Neural Mechanisms of Hypertension in Stroke-Prone Spontaneously Hypertensive Rats

Selenoprotein H Suppresses Cellular Senescence through Genome Maintenance and Redox Regulation

Oxidative Stress and Central Cardiovascular Regulation - Pathogenesis of Hypertension and Therapeutic Aspects -

Contact Info

Product

Resources

About