Effects of copper, cadmium and nickel on liver and kidney glutathione redox cycle of rats (Rattus sp.)

Cartañà, J.; Romeu, A; Arola, Lluı́s

doi:10.1016/0742-8413(92)90262-6

Cited by 30 publications

(12 citation statements)

References 20 publications

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“…Although previous studies have described the role of GSH in cellular resistance to metal toxicity, these studies have focused primarily on cadmium, mercury, and copper toxicity in cell lines (Kang and Enger, 1988;Freedman et al, 1989;Cartana et al, 1992;Steinebach and Wolterbeek, 1994;Hultberg et al, 1997). We were interested to determine the effect of GSH on the resistance to Cu and Fe (both reactive transition metals) in primary neurons.…”

Section: Discussionmentioning

confidence: 99%

Exacerbation of Copper Toxicity in Primary Neuronal Cultures Depleted of Cellular Glutathione

White

Bush

Beyreuther

et al. 1999

Journal of Neurochemistry

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Perturbations to glutathione (GSH) metabolism may play an important role in neurodegenerative disorders such as Alzheimer's, Parkinson's, and prion diseases. A primary function of GSH is to prevent the toxic interaction between free radicals and reactive transition metals such as copper (Cu). Due to the potential role of Cu in neurodegeneration, we examined the effect of GSH depletion on Cu toxicity in murine primary neuronal cultures. Depletion of cellular GSH with L-buthionine-[S,R]-sulfoximine resulted in a dramatic potentiation of Cu toxicity in neurons without effect on iron (Fe) toxicity. Similarly, inhibition of glutathione reductase (GR) activity with 1,3-bis(2-chloroethyl)-l -nitrosurea also increased Cu toxicity in neurons. To determine if the Alzheimer's amyloid-p (Ap) peptide can affect neuronal resistance to transition metal toxicity, we exposed cultures to nontoxic concentrations of Ap25-35 in the presence or absence of Cu or Fe. Ap25-35 pretreatment was found to deplete neuronal GSH and increase GR activity, confirming the ability of Ap to perturb neuronal GSH homeostasis.Ap25-35 pretreatment potently increased Cu toxicity but had no effect on Fe toxicity. These studies demonstrate an important role for neuronal GSH homeostasis in selective protection against Cu toxicity, a finding with widespread implications for neurodegenerative disorders.

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Section: Discussionmentioning

confidence: 99%

Exacerbation of Copper Toxicity in Primary Neuronal Cultures Depleted of Cellular Glutathione

White

Bush

Beyreuther

et al. 1999

Journal of Neurochemistry

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“…1) (Cartañ à et al, 1992;CEC, 1978;Friberg et al, 1974;Sullivan et al, 1984). The reason for such distribution is the high metallothionein synthesis in the liver (Friberg et al, 1986).…”

Section: Localization Of Cadmium In Tissuesmentioning

confidence: 92%

“…Glutathione (GSH; tripeptide thiol) is the second major cytosolic low-molecular-weight sulfhydryl compound that acts as a cellular reducing reagent and a protective reagent against numerous toxic substances including heavy metals through the -SH group (Cartañ à et al, 1992;Stryer, 1988). Glutathione has two forms: reduced (GSH), and oxidized (GSSG).…”

Section: Glutathionementioning

confidence: 99%

Cadmium distribution and toxicity in tissues of small rodents

Świergosz-Kowalewska

2001

Microscopy Res & Technique

110

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The aim of the present paper is to discuss the accumulation and distribution of cadmium (Cd) in the various tissues of animals, the interactions of cadmium with other elements, and the damage to tissues caused by this metal. Cadmium is not physiologically or biochemically essential to an organism. It is absorbed via the gastrointestinal tract and lungs and accumulated in various tissues, mainly the kidneys and liver. The distribution of cadmium between various tissues depends on many endogenous and exogenous factors. Cadmium is bound to a low-molecular-weight protein, metallothionein (MT), and to high-molecular-weight proteins. This metal has a great affinity to thiol groups. Cadmium binds also to O- and N-containing ligands. The distribution of cadmium between organs differs markedly depending on the chemical form of administered Cd and the duration of exposure. Acute exposure results in a different distribution pattern throughout the body than does chronic exposure. Long-term exposure to high doses of cadmium may cause biochemical and functional changes in some critical organs. Cadmium can influence the absorption and distribution of essential elements and can replace them in enzymes. Metallothionein and glutathione play important roles in the transport of metals and in detoxification processes. Reported findings are mainly the results of experiments on laboratory animals. The lack of data concerning the localization of cadmium in various tissues of wild species is noticeable and there is a great need for such data.

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“…The response of G6PDH, which also plays a role in antioxidant response (Cartañà et al, 1992), is nevertheless intriguing. The positive correlation observed here in the transcription levels of sod and g6pdh supports a coordinated antioxidant response.…”

Section: Temperature Effectsmentioning

confidence: 99%

Combined effects of temperature changes and metal contamination at different levels of biological organization in yellow perch

et al. 2016

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Effects of copper, cadmium and nickel on liver and kidney glutathione redox cycle of rats (Rattus sp.)

Cited by 30 publications

References 20 publications

Exacerbation of Copper Toxicity in Primary Neuronal Cultures Depleted of Cellular Glutathione

Exacerbation of Copper Toxicity in Primary Neuronal Cultures Depleted of Cellular Glutathione

Cadmium distribution and toxicity in tissues of small rodents

Combined effects of temperature changes and metal contamination at different levels of biological organization in yellow perch

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