Effects of age and dietary restriction on liver glutathione transferase activities in Lobund-Wistar rats

Chen, Linda H.; Hu, Naina; Snyder, David

doi:10.1016/0167-4943(94)90013-2

Cited by 14 publications

(13 citation statements)

References 30 publications

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“…NQO1 activity was significantly increased in CR-fed WT and KO liver cytosol compared with AL-fed WT and KO mice, respectively (P Ͻ 0.001 in both comparisons). In agreement with our findings, CR attenuated the age-related loss of antioxidative capacity due to aging and increased levels of NQO1 and GST in brain and liver, respectively (21)(22)(23). Liver homogenates from AL and 40% CR-fed WT and KO mice were tested.…”

supporting

confidence: 70%

“…However, CR has been shown to attenuate the age-related loss of antioxidative capacity due to aging and to increase levels of NQO1 and GST in brain and liver, respectively (21)(22)(23). The lack of functional Nrf2 in mice increases sensitivity to carcinogenesis through a lowered constitutive expression of antioxidative and detoxifying enzymes including NQO1 and GSTs (24)(25)(26).…”

mentioning

confidence: 99%

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Nrf2 mediates cancer protection but not prolongevity induced by caloric restriction

Pearson

Lewis

Price

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

214

156

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Caloric restriction (CR) is the most potent intervention known to both protect against carcinogenesis and extend lifespan in laboratory animals. A variety of anticarcinogens and CR mimetics induce and activate the NF-E2-related factor 2 (Nrf2) pathway. Nrf2, in turn, induces a number of antioxidative and carcinogendetoxifying enzymes. Thus, Nrf2 offers a promising target for anticarcinogenesis and antiaging interventions. We used Nrf2-disrupted (KO) mice to examine its role on the biological effects of CR. Here, we show that Nrf2 is responsible for most of the anticarcinogenic effects of CR, but is dispensable for increased insulin sensitivity and lifespan extension. Nrf2-deficient mice developed tumors more readily in response to carcinogen exposure than did WT mice, and CR was ineffective in suppressing tumors in the KO mice. However, CR extended lifespan and increased insulin sensitivity similarly in KO and WT mice. These findings identify a molecular pathway that dissociates the prolongevity and anticarcinogenic effects of CR.aging ͉ carcinogenesis ͉ oxidative stress

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supporting

confidence: 70%

mentioning

confidence: 99%

Nrf2 mediates cancer protection but not prolongevity induced by caloric restriction

Pearson

Lewis

Price

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

214

156

View full text Add to dashboard Cite

show abstract

“…Oxidative stress is postulated to be one of the most important mechanisms behind age-related decrease in SOD and GST activities in aging rats [15, 16]. Accordingly, many studies in the past attempted to clarify how these enzyme activities are altered during aging (for review, see [2, 17]).…”

Section: Introductionmentioning

confidence: 99%

Estradiol Modulates Membrane-Linked ATPases, Antioxidant Enzymes, Membrane Fluidity, Lipid Peroxidation, and Lipofuscin in Aged Rat Liver

Kumar

Kale

Baquer

2011

Journal of Aging Research

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Free radical production and oxidative stress are known to increase in liver during aging, and may contribute to the oxidative damage. These changes increase during menopausal condition in females when the level of estradiol is decreased. The objective of this study was to observe the changes in activities of membrane linked ATPases (Na+K+ ATPase, Ca2+ ATPase), antioxidant enzymes (superoxide dismutase, glutathione-S-transferase), lipid peroxidation levels, lipofuscin content and membrane fluidity occurring in livers of female rats of 3, 12 and 24 months age groups, and to see whether these changes are restored to 3 months control levels rats after exogenous administration of 17-β-estradiol (E2). The aged rats (12 and 24 months) were given subcutaneous injection of E2 (0.1 μg/g body weight) daily for one month. The results obtained in the present work revealed that normal aging was associated with significant decrease in the activities of membrane linked ATPases, antioxidant enzymes, membrane fluidity and an increase in lipid peroxidation and lipofuscin content in livers of aging female rats. The present study showed that E2 treatment reversed the changes to normal levels. E2 treatment may be beneficial in preventing some of the age related changes in the liver by increasing antioxidant defenses.

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“…In rats, expression of ␣, , and GST isoforms reached adult levels by postnatal day 10 (Tee et al, 1992). Studies of GST activities with several substrates, including 1-chloro-2,4-dinitrobenzene and 1,2-dichloro-4-nitrobenzene, in rats aged 6 to 30 months showed no changes in activity with 1-chloro-2,4-dinitrobenzene over this age range, but they showed a decline in activity with 1,2-dichloro-4-nitrobenzene at up to 30 months (Chen et al, 1994). In mice aged 8 to 10 weeks and 60 weeks, elimination of a single dose of DCA was reduced in 14-month-old control mice compared with 2-month old mice (Schultz et al, 2002).…”

mentioning

confidence: 99%

Age-Dependent Kinetics and Metabolism of Dichloroacetate: Possible Relevance to Toxicity

Shroads

Xu²,

Dixit³

et al. 2007

J Pharmacol Exp Ther

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Dichloroacetate (DCA) is an investigational drug for certain metabolic diseases. It is biotransformed principally by the -1 family isoform of glutathione transferase (GSTz1), also known as maleylacetoacetate isomerase (MAAI), which catalyzes the penultimate step in tyrosine catabolism. DCA causes a reversible peripheral neuropathy in several species, including humans. However, recent clinical trials indicate that adults are considerably more susceptible to this adverse effect than children. We evaluated the kinetics and biotransformation of DCA and its effects on tyrosine metabolism in nine patients treated for 6 months with 25 mg/kg/day and in rats treated for 5 days with 50 mg/kg/day. We also measured the activity and expression of hepatic GSTz1/MAAI. Chronic administration of DCA causes a striking age-dependent decrease in its plasma clearance and an increase in its plasma half-life in patients and rats. Urinary excretion of unchanged DCA in rats increases with age, whereas oxalate, an end product of DCA metabolism, shows the opposite trend. Low concentrations of monochloroacetate (MCA), which is known to be neurotoxic, increase as a function of age in the urine of dosed rats. MCA was detectable in plasma only of older animals. Hepatic GSTz1/MAAI-specific activity was inhibited equally by DCA treatment among all age groups, whereas plasma and urinary levels of maleylacetone, a natural substrate for this enzyme, increased with age. We conclude that age is an important variable in the in vivo metabolism and elimination of DCA and that it may account, in part, for the neurotoxicity of this compound in humans and other species.

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Effects of age and dietary restriction on liver glutathione transferase activities in Lobund-Wistar rats

Cited by 14 publications

References 30 publications

Nrf2 mediates cancer protection but not prolongevity induced by caloric restriction

Nrf2 mediates cancer protection but not prolongevity induced by caloric restriction

Estradiol Modulates Membrane-Linked ATPases, Antioxidant Enzymes, Membrane Fluidity, Lipid Peroxidation, and Lipofuscin in Aged Rat Liver

Age-Dependent Kinetics and Metabolism of Dichloroacetate: Possible Relevance to Toxicity

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