Induction of heat shock proteins and thermotolerance by ethanol in Saccharomycescerevisiae

Plesset, Judith; Palm, Curtis J.; McLaughlin, Calvin S.

doi:10.1016/0006-291x(82)92147-7

Cited by 187 publications

(92 citation statements)

References 14 publications

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“…Metallothionein, a protein in which Cys comprises 30% of the amino acid residues, is induced ten-fold at 24 hr after acute EtOH administration in young rats and mice [68][69][70]. Additionally, ethanol induces the rapid synthesis of stress proteins in young animals [71,72] while production of stress proteins is diminished in aging animals [73][74][75]. Thus, it is possible that in young animals, but less so in mature and old, an increase in protein synthesis occurs after exposure to high doses of EtOH, at the expense of GSH synthesis.…”

Section: Discussionmentioning

confidence: 99%

Glutathione depletion and recovery after acute ethanol administration in the aging mouse

Vogt

Richie

2007

Biochemical Pharmacology

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Glutathione (GSH) plays an important role in the detoxification of ethanol (EtOH) and acute EtOH administration leads to GSH depletion in the liver and other tissues. Aging is also associated with a progressive decline in GSH levels and impairment in GSH biosynthesis in many tissues. Thus, the present study was designed to examine the effects of aging on EtOH-induced depletion and recovery of GSH in different tissues of the C57Bl/6NNIA mouse. EtOH (2-5 g/kg) or saline was administered i.p. to mice of ages 6 mo (young), 12 mo (mature), and 24 mo (old); and GSH and cyst(e)ine concentrations were measured 0-24 hours thereafter. EtOH administration (5g/kg) depleted hepatic GSH levels >50% by 6 hr in all animals. By 24 hr, levels remained low in both young and old mice, but recovered to baseline levels in mature mice. At 6 hr, the decrease in hepatic GSH was dosedependent up to 3 g/kg EtOH, but not at higher doses. The extent of depletion at the 3 g/kg dose was dependent upon age, with old mice demonstrating significantly lower GSH levels than mature mice (P<0.001). Altogether these results indicate that aging was associated with a greater degree of EtOH and fasting-induced GSH depletion and subsequent impaired recovery in liver. An impaired ability to recover was also observed in young animals. Further studies are required to determine if an inability to recover from GSH depletion by EtOH is associated with enhanced toxicity.

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Section: Discussionmentioning

confidence: 99%

Glutathione depletion and recovery after acute ethanol administration in the aging mouse

Vogt

Richie

2007

Biochemical Pharmacology

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“…Exposure of an organ, tissue, or cells to a mild stress protects them against the effects of a subsequent equal or more severe stress (1,2). This preconditioning phenomenon has been observed in various organs such as the brain (3), skeletal muscle (4), liver (5), intestine (6), lung (7), and kidney (8).…”

Section: Introductionmentioning

confidence: 99%

Gentamicin-induced preconditioning of proximal tubular LLC-PK1 cells stimulates nitric oxide production but not the synthesis of heat shock protein

Pessoa

Convento

Silva

et al. 2009

Braz J Med Biol Res

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Nephrotoxicity is the main side effect of antibiotics such as gentamicin. Preconditioning has been reported to protect against injuries as ischemia/reperfusion. The objective of the present study was to determine the effect of preconditioning with gentamicin on LLC-PK1 cells. Preconditioning was induced in LLC-PK1 cells by 24-h exposure to 2.0 mM gentamicin (G/IU). After 4 or 15 days of preconditioning, cells were again exposed to gentamicin (2.0 mM) and compared to untreated control or G/ IU cells. Necrosis and apoptosis were assessed by acridine orange and HOESCHT 33346. Nitric oxide (NO) and endothelin-1 were assessed by the Griess method and available kit. Heat shock proteins were analyzed by Western blotting. After 15 days of preconditioning, LLC-PK1 cells exhibited a significant decrease in necrosis (23.5 ± 4.3 to 6.5 ± 0.3%) and apoptosis (23.5 ± 4.3 to 6.5 ± 2.1%) and an increase in cell proliferation compared to G/IU. NO (0.177 ± 0.05 to 0.368 ± 0.073 μg/mg protein) and endothelin-1 (1.88 ± 0.47 to 2.75 ± 0.53 pg/mL) production significantly increased after 15 days of preconditioning compared to G/IU. No difference in inducible HSP 70, constitutive HSC 70 or HSP 90 synthesis in tubular cells was observed after preconditioning with gentamicin. The present data suggest that preconditioning with gentamicin has protective effects on proximal tubular cells, that involved NO synthesis but not reduction of endothelin-1 or production of HSP 70, HSC 70, or HSP 90. We conclude that preconditioning could be a useful tool to prevent the nephrotoxicity induced by gentamicin.

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“…First, there is a temporal association between the development of thermotolerance and the appearance and disappearance of HSPs, whether induced by heat (18,25,29,34,36,44,48) or by other agents (30,45). This association also applies to preblastoderm embryos in which neither HSPs nor thermotolerance can be induced and in which the onset of thermotolerance corresponds to the inducibility of HSPs (21,37,47 (23,34,45).…”

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confidence: 99%

The major inducible heat shock protein hsp68 is not required for acquisition of thermal resistance in mouse plasmacytoma cell lines.

Aujame¹,

Firko²

1988

Mol. Cell. Biol.

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In mouse cells, the major inducible heat shock protein is a protein of 68,000 daltons (hsp68). We the whole cell population or true thermotolerance of a subpopulation), pretreatment usually stimulates the synthesis of HSPs, and a relationship between this synthesis and thermotolerance has been suggested (18,25,29,34, 36,48). A direct cause-effect relationship has yet to be clearly demonstrated, except possibly in Escherichia coli (55). Indeed, a number of recent studies have questioned the previous assumption that the synthesis of HSPs in eucaryotes is a requirement for the acquisition of thermotolerance (19,20,46,51,53).A genetic approach to the dissection of HSP function has been undertaken by a variety of groups (see, for example, references 14, 18, 24, and 42) with limited success. As a step in this direction, we have attempted to assess the contribution of the mouse major inducible HSP, hsp68, to thermotolerance in mouse plasmacytomas. In most mouse cells examined to date, hsp68 genes are stringently controlled; that is, they are essentially inactive except under stress. In mouse plasmacytomas, these genes cannot be activated, although other HSPs remain inducible (3,4

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Induction of heat shock proteins and thermotolerance by ethanol in Saccharomycescerevisiae

Cited by 187 publications

References 14 publications

Glutathione depletion and recovery after acute ethanol administration in the aging mouse

Glutathione depletion and recovery after acute ethanol administration in the aging mouse

Gentamicin-induced preconditioning of proximal tubular LLC-PK1 cells stimulates nitric oxide production but not the synthesis of heat shock protein

The major inducible heat shock protein hsp68 is not required for acquisition of thermal resistance in mouse plasmacytoma cell lines.

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