Effect of Age and Caloric Intake on Protein Oxidation in Different Brain Regions and on Behavioral Functions of the Mouse

Forster, Michael J.; Lal, Harbans; Sohal, Rajindar S.

doi:10.1006/abbi.1996.0380

Cited by 267 publications

(152 citation statements)

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“…Nevertheless, a pro-oxidizing shift in redox state and particularly the thiolation of proteins can induce a multiplicity of alterations in cellular functions. Amounts of reactive protein sulfhydryls, which were lower in SAM than in C57BL/6 mice, have been found previously to decrease in mouse tissues as function of age (Dubey et al, 1996). Loss of protein sulfhydryls is often associated with reversible thiolation of proteins.…”

Section: Discussionmentioning

confidence: 92%

Comparison of thiol redox state of mitochondria and homogenates of various tissues between two strains of mice with different longevities

Rebrin

Sohal

2004

Experimental Gerontology

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The main purpose of this study was to determine if differences in life spans of two different strains of mice are associated with the thiol redox state of their tissues and mitochondria. A comparison, based on amounts of reduced and oxidized glutathione (GSH, GSSG) and reactive protein thiols, was made between short-lived SAM (P8) mice and the longer-lived C57BL/6 mice at 13 months of age. The average life span of the latter mouse strain is approximately 48% longer than the former strain. Analyses of plasma, tissue homogenates and mitochondria of liver, kidney, heart, brain and skeletal muscle indicated that, in general, amounts of GSH and reactive protein sulfhydryls and GSH:GSSG ratios were lower and concentrations of GSSG were higher in the SAM than the C57BL/6 mice. Differences in the redox state between the two strains were more consistent and pronounced in skeletal muscle than in other tissues, and in mitochondria than in their respective tissue homogenates. Overall, the results support the view that the shorter-lived SAM mice exhibit a relatively higher level of oxidative stress than the longer-lived C57BL/6 mice, which is consistent with the predictions of the oxidative stress hypothesis of aging. Intra-species comparisons may be useful for the identification of biochemical characteristics associated with the variations in life spans.

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Section: Discussionmentioning

confidence: 92%

Comparison of thiol redox state of mitochondria and homogenates of various tissues between two strains of mice with different longevities

Rebrin

Sohal

2004

Experimental Gerontology

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“…Previous studies on ageassociated oxidative damage yielded a similar pattern of changes. Dubey et al (1996) reported age-related increases in protein oxidation in several regions of the forebrain, most notably in the hippocampus and striatum, whereas no change was observed in the brainstem. Such oxidative damage to proteins would seem to have functional implications, as suggested by the correlation of the severity of the damage with cognitive or motor performance of aged mice or rats Nicolle et al, 2001).…”

Section: Discussionmentioning

confidence: 98%

Effects of age and caloric intake on glutathione redox state in different brain regions of C57BL/6 and DBA/2 mice

2007

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The main purpose of the present study was to determine whether specific regions of the mouse brain exhibit different age-related changes in oxidative stress, as indicated by glutathione redox state and the level of protein-glutathionyl mixed disulfides. Comparison of 3-and 21-month-old mice indicated an age-related decrease in the ratio of reduced to oxidized glutathione (GSH:GSSG) as well as a prooxidizing shift in the calculated redox potential (ranging from 6 to 15 mV) in the cortex, hippocampus, striatum and cerebellum, whereas there was little change in the brainstem. This pro-oxidizing shift in redox state was due to a modest decrease in GSH content occurring in all the brain regions examined, and elevations in GSSG amount that were most pronounced in the striatum and cerebellum. The regional changes in glutathione redox state were paralleled by increases in the amounts of protein-mixed disulfides. A reduction of caloric intake by 40% for a short period (7 weeks), implemented in relatively old mice (17 months), increased the GSH:GSSG ratio and redox potential at 19 months in the same brain regions that exhibited age-related decreases. The effects of age and caloric restriction were qualitatively similar in C57BL/6 and DBA/2 mice. However, young DBA/2 mice, which do not show extension of life span in response to long-term caloric restriction, had lower GSH:GSSG ratios and higher protein-mixed disulfides than age-matched C57BL/6 mice. The current findings demonstrate that oxidative stress, as reflected by glutathione redox state, increases in the aging brain in regions linked to age-associated losses of function and neurodegenerative diseases.

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“…The brain regions studied in this project -cerebral cortex, striatum, midbrain, and hippocampus -are involved in pain processing (Basbaum and Jessell, 2000), express opioid receptors (Pasternak, 1993, Zastawny et al, 1994, and, moreover, oxidative damage to proteins and lipids in these brain regions increase markedly with aging (Dubey et al, 1996, Forster et al, 2000, Liu et al, 2002, Rebrin et al 2007). Recently, it was reported that reactive oxygen species play a mediatory role in spinal injury-induced pain (Crisp et al, 2006, Hacimuftuolgu et al, 2006.…”

Section: Discussionmentioning

confidence: 99%

“…The aging process is associated with cellular damage caused by reactive oxygen species. There was a significant increase in protein oxidation in aged mice brain regions such as the cortex, hippocampus, striatum, and midbrain (Dubey et al, 1996, Forster et al, 2000, Rebrin et al 2007), but a minimal or no change in the brainstem (Rebrin et al 2007). The cortex, striatum, hippocampus, and midbrain express opioid receptors (Delfs, 1994, Mansour et al, 1988, Pasternak, 1993, Zastawny et al, 1994 and contribute to pain processing (Basbaum and Jessell, 2000), therefore age-related oxidative damage in these regions may affect pain sensitivity and opioid analgesia.…”

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confidence: 95%

Oxidative damage and sensitivity to nociceptive stimulus and opioids in aging rats

Raut

Ratka

2009

Neurobiology of Aging

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Oxidative stress contributes to aging and may cause alterations in pain and analgesia. Knowledge about effects of oxidative stress on the opioid system is very limited. This project was designed to determine the relationship between age-related oxidative damage and opioid antinocicpetion. Three age groups of male Fischer 344 rats were tested for pain sensitivity and responses to morphine and fentanyl using the hot plate method. Oxidative stress markers in various brain regions were measured. With advancing age, nociceptive threshold and antinociceptive effects of opioids decreased significantly. There was a significant negative correlation between morphine antinociception and protein oxidation in cortex, striatum, and midbrain (r 2 = 0.73, 0.87, and 0.77, respectively), and lipid peroxidation in cerebral cortex, hippocampus, and striatum (r 2 = 0.73, 0.61 and 0.71, respectively). Similar correlation was observed between oxidative stress markers and fentanyl antinociception. These findings demonstrate that the age-related increase in oxidative damage in brain is associated with a significant decrease in the antinociceptive effects of opioids.

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Effect of Age and Caloric Intake on Protein Oxidation in Different Brain Regions and on Behavioral Functions of the Mouse

Cited by 267 publications

References 0 publications

Comparison of thiol redox state of mitochondria and homogenates of various tissues between two strains of mice with different longevities

Comparison of thiol redox state of mitochondria and homogenates of various tissues between two strains of mice with different longevities

Effects of age and caloric intake on glutathione redox state in different brain regions of C57BL/6 and DBA/2 mice

Oxidative damage and sensitivity to nociceptive stimulus and opioids in aging rats

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