Time- and dose-dependent inhibition of erythrocyte glutathione peroxidase by cisplatin

Milano, G.; Caldani, C.; Khater, R.; Launay, Jean‐Marie; Soummer, Anne-Marie; Namer, M.; Schneider, M.

doi:10.1016/0006-2952(88)90196-7

Cited by 22 publications

(6 citation statements)

References 11 publications

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“…Therefore, a decrease in the glutathione peroxidase activity could cause accumulation of H20 2 and lipid hydroperoxides, thus leading to deleterious effects. These results correlate well with those of Vernie et al [38] and Milano et al [39] who showed that cisplatin inhibited erythrocyte glutathione peroxidase, and with those re cently published by Hannemann and Baumann [40], Maines [30] did not reveal any effect of cisplatin treat ment on GSH content nor on glutathione reductase activ ity in the kidney. This discrepancy may be explained by the difference in the rat strains used and the treatment regimen (see above).…”

Section: Discussionsupporting

confidence: 82%

Cisplatin Nephrotoxicity in Cadmium-Pretreated Rats

Bompart¹,

Orfila²,

Manuel³

1991

Nephron

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Treatment of rats with cisplatin or with cisplatin after chronic pre-exposure to cadmium induced a decrease in kidney cytochrome P-450 and glutathione levels, and in glutathione peroxidase and reductase activities. Furthermore, cadmium and cisplatin enhanced lipid peroxidation, oxidized glutathione and N-glucuronyl transferase activity. Glutathione S-transferase (substrate: 1-chloro-2,4-dinitrobenzene) was increased and decreased by cadmium and cisplatin respectively. On morphological observation, cadmium nephrotoxicity was characterized by tubular proximal damage with mitochondrial and lysosomal changes and a widespread vesiculation of tubular cells. A marked focal tubular necrosis associated with cyst formation was observed in cisplatin nephrotoxicity. On the basis of the measured biochemical, functional and histological parameters, it is concluded that cadmium pretreatment did not potentiate the nephrotoxic effect of cisplatin.

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Section: Discussionsupporting

confidence: 82%

Cisplatin Nephrotoxicity in Cadmium-Pretreated Rats

Bompart¹,

Orfila²,

Manuel³

1991

Nephron

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“…We found that GRd and GPx activities decreased significantly in PKU when compared to controls whereas GSSG increased, probably due to the low activity in GRd. Because of the sensitivity of these enzymes toward environmental pollutants and drugs (Milano et al, 1988; Vernie et al, 1988), they have been used as markers of their toxic effects, oxidative stress and cell integrity. GPx plays a role in the destruction of hydrogen peroxide and lipid hydroperoxides (Weiss et al, 1980; Wendel, 1981) generated by enzymatic and nonenzymatic reactions in cells.…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress induced by phenylketonuria in the rat: Prevention by melatonin, vitamin E, and vitamin C

Martinez-Cruz

Pozo

Osuna

et al. 2002

J of Neuroscience Research

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Phenylketonuria (PKU) is an autosomal recessive disorder caused by a deficiency of the phenylalanine hydroxylation system and is characterized by a block in the conversion of phenylalanine (PHE) to tyrosine. We examined the effects of maternal hyperphenylalaninemia on the morphological and biochemical development of pup rat brain and cerebellum. In our model of PKU we evaluated a number of markers of oxidative stress such as Ehrlich adducts formation, lipid peroxidation, as well as the levels of reduced and oxidized glutathione, and the activities of the enzymes glutathione peroxidase and glutathione reductase. We also studied the expression of heme-oxigenase-1 and mitogen-activated protein kinase 1/2 (MAPK 1/2) as additional markers of oxidative stress. We demonstrate that PKU strongly increased most of the oxidative stress markers studied and induced significant morphological damage. We also showed that daily administration of melatonin (20 mg/kg BW), vitamin E (30 mg/kg BW), and vitamin C (30 mg/kg BW) until delivery prevented the oxidative biomolecular damage in the rat brain and cerebellum. Although no significant differences were observed among the antioxidants studied, it should be noted that the doses of melatonin were less than those for vitamins E and C. We conclude that PKU induces a clear state of oxidative stress that is somehow involved in the brain and body damage occurring in this inborn error. Moreover, melatonin and other antioxidants are capable of preventing completely the damage induced by PKU.

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“…A .). Notably, human GSH reductase, which has a strong homology to human TrxR and contains a similar redox-active disulfide/dithiol moiety but no seleno-cysteine residue, is not inhibited by cisplatin (16, 251, 404, 405). Therefore, the highly reactive seleno-cysteine residue at the C-terminal domain was suggested to be the TrxR target of cisplatin (405).…”

Section: Metal-based Anticancer Drugs and Their Redox-related Modementioning

confidence: 99%

Anticancer Activity of Metal Complexes: Involvement of Redox Processes

Jungwirth

Kowol

Keppler

et al. 2011

Antioxidants & Redox Signaling

460

357

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Cells require tight regulation of the intracellular redox balance and consequently of reactive oxygen species for proper redox signaling and maintenance of metal (e.g., of iron and copper) homeostasis. In several diseases, including cancer, this balance is disturbed. Therefore, anticancer drugs targeting the redox systems, for example, glutathione and thioredoxin, have entered focus of interest. Anticancer metal complexes (platinum, gold, arsenic, ruthenium, rhodium, copper, vanadium, cobalt, manganese, gadolinium, and molybdenum) have been shown to strongly interact with or even disturb cellular redox homeostasis. In this context, especially the hypothesis of "activation by reduction" as well as the "hard and soft acids and bases" theory with respect to coordination of metal ions to cellular ligands represent important concepts to understand the molecular modes of action of anticancer metal drugs. The aim of this review is to highlight specific interactions of metal-based anticancer drugs with the cellular redox homeostasis and to explain this behavior by considering chemical properties of the respective anticancer metal complexes currently either in (pre)clinical development or in daily clinical routine in oncology.

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Time- and dose-dependent inhibition of erythrocyte glutathione peroxidase by cisplatin

Cited by 22 publications

References 11 publications

Cisplatin Nephrotoxicity in Cadmium-Pretreated Rats

Cisplatin Nephrotoxicity in Cadmium-Pretreated Rats

Oxidative stress induced by phenylketonuria in the rat: Prevention by melatonin, vitamin E, and vitamin C

Anticancer Activity of Metal Complexes: Involvement of Redox Processes

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