Age‐related acute depletion of cerebral glutathione by peroxidative stress

Benzi, G.; Curti, Daniela; Marzatico, Fulvio; Pastoris, Ornella

doi:10.1002/jnr.490290413

Cited by 18 publications

(3 citation statements)

References 29 publications

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“…The significant decrease in GSH activity by cadmium could be due to either increased use of GSH in the scavenging of free radicals that were produced by Cd or increased utilization of GSH for the activity of GPx forming oxidized GSH (GSSG) due to increased generation of ROS (46). Chronic pre-treatment with phosphatidylcholine partially inhibits GSH depletion in the forebrains of aged rats (47), suggesting that alterations in the phospholipid composition of the mitochondrial inner membrane and/or cytochrome oxidase activity might play a role in oxygen free radical production. Additionally, vitamin E neutralizes lipid peroxidation and unsaturated membrane lipids because of its free radical scavenging activity (48).…”

Section: Photomicrographs Of the Kidneysmentioning

confidence: 99%

Livolin Forte Ameliorates Cadmium-Induced Kidney Injury in Wistar Rats

Akomolafe

Imafidon

Olukiran

et al. 2016

Serbian Journal of Experimental and Clinical Research

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Th e kidney, which is an integral part of the drug excretion system, was reported as one of the targets of cadmium toxicity. Early events of cadmium toxicity in the cell include a decrease in cell membrane fl uidity, breakdown of its integrity, and impairment of its repair mechanisms. Phosphatidylcholine and vitamin E have a marked fl uidizing eff ect on cellular membranes. We hypothesized that Livolin forte® (LIV) could attenuate kidney damage induced by cadmium in rats. Twenty-fi ve adult male Wistar rats were divided into fi ve groups of fi ve rats each: group I (control group) received 0.3 ml/kg/day of propylene glycol for six weeks; group II was given 5 mg/kg/day of cadmium (Cd) i.p for 5 consecutive days; group III rats were treated in a similar way as group II but were allowed a recovery period of 4 weeks; group IV was treated with LIV (5.2 mg/kg/day) for a period of 4 weeks after inducing renal injury with Cd similarly to group II; and group V was allowed a recovery period of 2 weeks after a 4-week LIV treatment (5.2 mg/kg/day) following Cd administration. A significant increase in plasma creatinine, urea, uric acid, and TBARS were observed in groups II and III compared to the control rats. Signifi cant reductions in total protein, glucose, and GSH activity were also recorded. Th e urine concentrations of creatinine, urea, and uric acid in groups II and III were signifi cantly lower than the control group. Th is fi nding was accompanied by a signifi cant decrease in creatinine and urea clearance. Post-treatment with LIV caused signifi cant decreases in plasma creatinine, urea, uric acid, and TBARS. Signifi cant increases in total protein, glucose, and GSH activity of groups IV and V were observed compared to group II. A signifi cant increase in urine concentrations of creatinine, urea, and uric acid and signifi cant decreases in total protein, glucose, and GSH activity were observed in groups IV and V compared to group II. Photomicrographs of the rat kidneys in groups IV and V showed an improvement in the histology of their renal tissue when compared to group II, with features similar to the control rats. Additionally, group III showed an improvement in the histoarchitecture of the kidney compared with group II, although occasional atrophy of some glomeruli and shrinking of renal corpuscles was observed.

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Section: Photomicrographs Of the Kidneysmentioning

confidence: 99%

Livolin Forte Ameliorates Cadmium-Induced Kidney Injury in Wistar Rats

Akomolafe

Imafidon

Olukiran

et al. 2016

Serbian Journal of Experimental and Clinical Research

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“…Although the bulk of the dry matter of the inner mitochondria1 membrane is protein (Harmon et al, 1974), a direct relationship exists between the amount of negatively charged phospholipids and the catalytic activity of cytochrome oxidase (Vik and Capaldi, 1977;Fry and Green, 1980;Casanovas et al, 1985). In old rats, the chronic pretreatment with phosphatidylcholine partially inhibits the reduced glutathione depletion by prooxidants, suggesting that the alteration in mitochondrial inner membrane phospholipid composition might play a role in oxygen free-radical production (Benzi et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

Effect of intermittent mild hypoxia and drug treatment on synaptosomal nonmitochondrial ATPase activities

Benzi

Gorini

Arnaboldi

et al. 1993

J of Neuroscience Research

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Synaptosomal nonmitochondrial ATPases linked to the energy-utilizing systems were evaluated in cerebral cortex from normoxic rats and rats submitted to mild intermittent normobaric hypoxia [12 hr daily exposure to N2:O2 (90:10) mixture for 4 weeks]. The activities of Na+,K(+)-ATPase; high- and low-affinity Ca(2+)-ATPase; basal Mg(2+)-ATPase; and Ca2+, Mg(2+)-ATPase were assayed in synaptosomes and synaptosomal subfractions, namely, synaptosomal plasma membranes and synaptic vesicles. The evaluations were performed either in normoxic rats or in hypoxic rats submitted to 4-week treatment with saline (controls) or a vasodilator agent (papaverine), an energy-metabolism interfering agent (theniloxazine), a calcium blocker (nicardipine), and a lipid-metabolism interfering agent (phosphatidylcholine) in order to define the plasticity and the selective changes in individual ATPases. In synaptosomes from rat cerebral cortex, the enzyme adaptation to the daily mild intermittent hypoxia for 4 weeks was characterized by an increase in the activity of Mg(2+)-ATPase, concomitant with a decrease in the activities of Na+,K(+)-ATPase, high-affinity Ca(2+)-ATPase, and Ca2+, Mg(2+)-ATPase. In hypoxic rats the enzyme adaptation to the 4-week treatment with phosphatidylcholine was characterized by an increase in Ca2+, Mg(2+)-ATPase activity and a decrease in Mg(2+)-ATPase activity. The action involves the enzymatic form located in the synaptic plasma membranes. In hypoxic rats the adaptation to the 4 week treatment with nicardipine was characterized by an increase in high-affinity Ca(2+)-ATPase activity, while the 4-week-treatment with theniloxazine induced an increase in Na+,K(+)-ATPase activity. The actions of both nicardipine and theniloxazine were related to the enzymatic forms located in the synaptic plasma membranes. The effects on the biophase induced by the sequential cycles of hypoxia/normoxia and the treatment with the various agents tested should also be related to the changes induced in the activity of some synaptosomal ATPases.

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“…Endogenous glutathione levels could be decreased by different compounds that: (1) oxidize GSH to GSSG; (2) alkylate GSH as a sulfhydryl reactant; (3) inhibit glutathione synthesis; and (4) conjugate with glutathione through their electrophilic sites (Masukawa et al . 1989; Benzi et al . 1991).…”

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confidence: 99%

Effects of glutathione depletion by 2‐cyclohexen‐1‐one on excitatory amino acids‐induced enhancement of activator protein‐1 DNA binding in murine hippocampus

Ogita

Kitayama

Okuda

et al. 2001

Journal of Neurochemistry

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We have investigated the role of glutathione in mechanisms associated with excitatory amino acid signaling to the nuclear transcription factor activator protein-1 (AP1) in the brain using mice depleted of endogenous glutathione by prior treatment with 2-cyclohexen-1-one (CHX). In the hippocampus of animals treated with CHX 2 h before, a signi®cant increase was seen in enhancement of AP1 DNA binding when determined 2 h after the injection of kainic acid (KA) at low doses. The sensitization to KA was not seen in animals injected with CHX 24 h before, in coincidence with the recovery of glutathione contents to the normal levels. By contrast, CHX did not signi®cantly affect the potentiation by NMDA of AP1 binding under any experimental conditions. Prior treatment with CHX resulted in facilitation of behavioral changes induced by KA without affecting those induced by NMDA. These results suggest that endogenous glutathione may be at least in part involved in molecular mechanisms underlying transcriptional control by KA, but not by NMDA, signals of cellular functions.

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Age‐related acute depletion of cerebral glutathione by peroxidative stress

Cited by 18 publications

References 29 publications

Livolin Forte Ameliorates Cadmium-Induced Kidney Injury in Wistar Rats

Livolin Forte Ameliorates Cadmium-Induced Kidney Injury in Wistar Rats

Effect of intermittent mild hypoxia and drug treatment on synaptosomal nonmitochondrial ATPase activities

Effects of glutathione depletion by 2‐cyclohexen‐1‐one on excitatory amino acids‐induced enhancement of activator protein‐1 DNA binding in murine hippocampus

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