J Clin Epidemiol. 47(9):1021-6,1994
Glutathione and morbidity in a community-based sample of elderly.
It is well known that aging is accompanied by a precipitous fall in glutathione levels. Lower glutathione levels are implicated in many diseases associated with aging, including cataracts, Alzheimer’s disease, Parkinson’s, atherosclerosis and others.
Adv Drug Deliv Rev. 2008 Oct-Nov;60(13-14):1545-52
Pro-oxidant shift in glutathione redox state during aging.
Abstract
The GSH:GSSG ratio, which is the primary determinant of the cellular redox state, becomes progressively more pro-oxidizing during the aging process due to an elevation in the GSSG content and a decline in the ability for de novo GSH biosynthesis. The K(m) of glutamate-cysteine ligase (GCL), the rate-limiting enzyme in de novo GSH biosynthesis, significantly increases during aging, which would adversely affect the ability for rapid GSH biosynthesis, especially under stressful conditions. Experimental studies suggest that age-related accumulation of homocysteine, an intermediate in the trans-sulfuration pathway, may be responsible for causing the loss of affinity between GCL and its substrates. Over-expression of GCL has been shown to prolong the life span of Drosophila by up to 50%, suggesting that perturbations in glutathione metabolism play a causal role in the aging process.
J Hum Hypertens. 2005 Dec;19(12):951-69.
Contributions of the sympathetic nervous system, glutathione, body mass and gender to blood pressure increase with normal aging: influence of heredity.
Abstract
Body mass and sympathetic activity increase with aging and might underlie blood pressure (BP) elevation. Increased body mass index (BMI) may elevate BP by increasing sympathetic activity. Glutathione (GSH) can decrease BP, and declines with aging. We measured systolic (SBP) and diastolic BP, BMI, plasma (NE(pl)) and urine norepinephrine (NEu), and plasma GSH in n=204 twins across the age spectrum. BP correlated directly with BMI, NEpl, and NEu, but inversely with GSH. Age correlated with BP, BMI, NEpl, and NEu. BP, BMI, NEpl, and NEu were higher in older subjects than younger subjects, whereas GSH was lower with aging. In older subjects with high (above median) NEpl, SBP was 8 mmHg higher than in those of comparable age with low NE. In younger subjects with high GSH, BP was significantly lower than in younger subjects having low GSH. NEu was significantly reduced in young high-BMI subjects vs young low-BMI subjects. The heritability (h2) of NEpl, NEu, and GSH ranged from approximately 50 to approximately 70%, and these biochemical quantities were considerably more heritable than BP. We conclude that increases in sympathetic activity contribute to aging-induced SBP elevations, especially in older females. GSH reductions apparently participate in aging-induced BP elevations, most strongly in males. BMI increases contribute to BP elevations, particularly in younger subjects. BMI elevations apparently raise BP mainly by peripheral mechanisms, with generally little sympathetic activation. Substantial h(2) for plasma GSH, NE, and urine NE suggests that such traits may be useful 'intermediate phenotypes' in the search for genetic determinants of BP.
Antioxid Redox Signal. 2013 Sep 10;19(8):813-22.
Functional consequences of age-dependent changes in glutathione status in the brain.
Abstract
SIGNIFICANCE:
A decline in both cognitive and motor functions is one of the characteristics of aging. This results in changes in learning and memory, as well as deficits in balance and coordination that significantly impact the quality of life. Importantly, age is the greatest risk factor for a number of neurodegenerative diseases. Alterations in redox homeostasis, protein modification and processing, mitochondrial function, and the immune response have all been implicated in the decline of the aging brain.
RECENT ADVANCES:
Brain glutathione (GSH) decreases with age in humans, and a loss of GSH can impact cognitive function. Decreases in GSH are also associated with microglial activation and endothelial dysfunction, both of which can contribute to impairments in brain function. Changes in redox homeostasis can also potentiate the accumulation of advanced glycation endproducts, resulting in defects in protein processing and function as well as a further increase in inflammation.
CRITICAL ISSUES:
We argue here that many of the changes in brain function associated with age are linked through GSH metabolism.
FUTURE DIRECTIONS:
Further research focused on better understanding how age affects GSH homeostasis with a particular emphasis on the key transcription factors involved in GSH metabolism is needed.
Glutathione and morbidity in a community-based sample of elderly.
เป็นที่ทราบกันดีว่าเมื่อคนเรามีอายุสูงขึ้นระดับกลูทาไธโอนจะลดลงอย่างรวดเร็ว ระดับกลูทาไธโอนที่ต่ำลงมีความสัมพันธ์กับการเกิดโรคภัยไข้เจ็บในผู้สูงอายุได้แก่ ต้อกระจก อัลไซม์เมอร์ พาร์กินสัน โรคหลอดเลือดหัวใจอุดตัน เป็นต้น
It is well known that aging is accompanied by a precipitous fall in glutathione levels. Lower glutathione levels are implicated in many diseases associated with aging, including cataracts, Alzheimer’s disease, Parkinson’s, atherosclerosis and others.
Adv Drug Deliv Rev. 2008 Oct-Nov;60(13-14):1545-52
Pro-oxidant shift in glutathione redox state during aging.
Abstract
The GSH:GSSG ratio, which is the primary determinant of the cellular redox state, becomes progressively more pro-oxidizing during the aging process due to an elevation in the GSSG content and a decline in the ability for de novo GSH biosynthesis. The K(m) of glutamate-cysteine ligase (GCL), the rate-limiting enzyme in de novo GSH biosynthesis, significantly increases during aging, which would adversely affect the ability for rapid GSH biosynthesis, especially under stressful conditions. Experimental studies suggest that age-related accumulation of homocysteine, an intermediate in the trans-sulfuration pathway, may be responsible for causing the loss of affinity between GCL and its substrates. Over-expression of GCL has been shown to prolong the life span of Drosophila by up to 50%, suggesting that perturbations in glutathione metabolism play a causal role in the aging process.
J Hum Hypertens. 2005 Dec;19(12):951-69.
Contributions of the sympathetic nervous system, glutathione, body mass and gender to blood pressure increase with normal aging: influence of heredity.
Abstract
Body mass and sympathetic activity increase with aging and might underlie blood pressure (BP) elevation. Increased body mass index (BMI) may elevate BP by increasing sympathetic activity. Glutathione (GSH) can decrease BP, and declines with aging. We measured systolic (SBP) and diastolic BP, BMI, plasma (NE(pl)) and urine norepinephrine (NEu), and plasma GSH in n=204 twins across the age spectrum. BP correlated directly with BMI, NEpl, and NEu, but inversely with GSH. Age correlated with BP, BMI, NEpl, and NEu. BP, BMI, NEpl, and NEu were higher in older subjects than younger subjects, whereas GSH was lower with aging. In older subjects with high (above median) NEpl, SBP was 8 mmHg higher than in those of comparable age with low NE. In younger subjects with high GSH, BP was significantly lower than in younger subjects having low GSH. NEu was significantly reduced in young high-BMI subjects vs young low-BMI subjects. The heritability (h2) of NEpl, NEu, and GSH ranged from approximately 50 to approximately 70%, and these biochemical quantities were considerably more heritable than BP. We conclude that increases in sympathetic activity contribute to aging-induced SBP elevations, especially in older females. GSH reductions apparently participate in aging-induced BP elevations, most strongly in males. BMI increases contribute to BP elevations, particularly in younger subjects. BMI elevations apparently raise BP mainly by peripheral mechanisms, with generally little sympathetic activation. Substantial h(2) for plasma GSH, NE, and urine NE suggests that such traits may be useful 'intermediate phenotypes' in the search for genetic determinants of BP.
Antioxid Redox Signal. 2013 Sep 10;19(8):813-22.
Functional consequences of age-dependent changes in glutathione status in the brain.
Abstract
SIGNIFICANCE:
A decline in both cognitive and motor functions is one of the characteristics of aging. This results in changes in learning and memory, as well as deficits in balance and coordination that significantly impact the quality of life. Importantly, age is the greatest risk factor for a number of neurodegenerative diseases. Alterations in redox homeostasis, protein modification and processing, mitochondrial function, and the immune response have all been implicated in the decline of the aging brain.
RECENT ADVANCES:
Brain glutathione (GSH) decreases with age in humans, and a loss of GSH can impact cognitive function. Decreases in GSH are also associated with microglial activation and endothelial dysfunction, both of which can contribute to impairments in brain function. Changes in redox homeostasis can also potentiate the accumulation of advanced glycation endproducts, resulting in defects in protein processing and function as well as a further increase in inflammation.
CRITICAL ISSUES:
We argue here that many of the changes in brain function associated with age are linked through GSH metabolism.
FUTURE DIRECTIONS:
Further research focused on better understanding how age affects GSH homeostasis with a particular emphasis on the key transcription factors involved in GSH metabolism is needed.
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