Stress Proteins and SH-Groups in Oxidant-Induced Cellular Injury After Chronic Ethanol Administration in Rat

Calabrese, Vittorio; Renis, Marcella; Calderone, Agata; Russo, Alessandra; Reale, S.; Barcellona, Maria Luisa; Rizza, V.

doi:10.1016/s0891-5849(97)00441-3

Cited by 91 publications

(50 citation statements)

References 39 publications

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“…In the brain, the amount of Hsp70 protein correlated negatively with the level of lipid peroxidation; the cerebellum and hippocampus displayed the lowest levels of lipid peroxidation, with the highest Hsp70 induction (Calabrese et al 1996). Chronic (12-week) ethanol administration was found to increase the level of Hsp70 in these cerebral areas and in the liver (Calabrese et al 1998). Chronic ethanol consumption similarly led to an increased expression level of Hsp70 in the amygdala (Bell et al 2006).…”

Section: Heat Shock Proteins and Their Roles In Membrane Protectionmentioning

confidence: 95%

“…An elevated level of Hsp70 expression related to ethanol-induced liver injury has been observed in rats (Nanji et al 1995), and maternal ethanol consumption likewise resulted in an elevated level of Hsp70 in different brain regions of rat pups (Holownia et al 1995). Both acute and chronic ethanol treatment induces the expression of Hsp70 in the brain and liver of rats (Calabrese et al 1996;Calabrese et al 1998). Acute administration of 5 g/kg ethanol resulted in an increased level of Hsp70 in the hippocampus, cerebellum, cortex, striatum, and liver.…”

Section: Heat Shock Proteins and Their Roles In Membrane Protectionmentioning

confidence: 96%

“…Both in vitro ethanol addition and chronic alcohol consumption have been demonstrated to lead to the enhanced formation of ROS and increased lipid peroxidation in the rat brain (Montoliu et al 1994). Higher levels of lipid peroxidation in different brain regions and also in the liver were measured after both acute and chronic ethanol administrations in rats (Calabrese et al 1996;Calabrese et al 1998). The short-term ethanol treatment of cultured fetal rat cortical neurons resulted in increased ROS formation and a decreased level of glutathione followed by apoptosis (Rathinam et al 2006).…”

Section: The Effects Of Alcohol On Cellular Physiologymentioning

confidence: 98%

“…The short-term ethanol treatment of cultured fetal rat cortical neurons resulted in increased ROS formation and a decreased level of glutathione followed by apoptosis (Rathinam et al 2006). Chronic ethanol feeding decreased the activity levels of SOD-1 and SOD-2 in the brain (Calabrese et al 1998). The brain is especially sensitive to oxidative injury, due to its high oxygen consumption, the high content of polyunsaturated fatty acid side chains in the neuronal membranes, and the weak antioxidant system in most brain regions (Halliwell 2006).…”

Section: The Effects Of Alcohol On Cellular Physiologymentioning

confidence: 99%

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Alcohol stress, membranes, and chaperones

Tóth

Vı́gh

Sántha

2014

Cell Stress and Chaperones

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Ethanol, which affects all body organs, exerts a number of cytotoxic effects, most of them independent of cell type. Ethanol treatment leads to increased membrane fluidity and to changes in membrane protein composition. It can also interact directly with membrane proteins, causing conformational changes and thereby influencing their function. The cytotoxic action may include an increased level of oxidative stress. Heat shock protein molecular chaperones are ubiquitously expressed evolutionarily conserved proteins which serve as critical regulators of cellular homeostasis. Heat shock proteins can be induced by various forms of stresses such as elevated temperature, alcohol treatment, or ischemia, and they are also upregulated in certain pathological conditions. As heat shock and ethanol stress provoke similar responses, it is likely that heat shock protein activation also has a role in the protection of membranes and other cellular components during alcohol stress.

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Section: Heat Shock Proteins and Their Roles In Membrane Protectionmentioning

confidence: 95%

Section: Heat Shock Proteins and Their Roles In Membrane Protectionmentioning

confidence: 96%

Section: The Effects Of Alcohol On Cellular Physiologymentioning

confidence: 98%

Section: The Effects Of Alcohol On Cellular Physiologymentioning

confidence: 99%

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Alcohol stress, membranes, and chaperones

Tóth

Vı́gh

Sántha

2014

Cell Stress and Chaperones

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“…α-Lipoic acid (LA) is an essential cofactor in mitochondrial dehydrogenase reactions, functions as an antioxidant and reduces oxidative stress in aged animals (16). LA and its reduced form, dihydrolipoic acid (DHLA), protects neuronal cultures from oxidative stress, when treated with amyloid beta-peptide (Abeta [25][26][27][28][29][30][31][32][33][34][35] and iron/hydrogen peroxide [Fe/H 2 O 2 ] (17). Therefore, in the present study, we evaluated the role of ALCAR and LA co-treatment, to demonstrate its possible protective effects against HNE-induced oxidative stress and neurotoxicity in cortical neuronal cells.…”

Section: Introductionmentioning

confidence: 99%

Involvement of PI3K/PKG/ERK1/2 signaling pathways in cortical neurons to trigger protection by cotreatment of acetyl-L-carnitine and α-lipoic acid against HNE-mediated oxidative stress and neurotoxicity: Implications for Alzheimer's disease

Abdul

Butterfield

2007

Free Radical Biology and Medicine

126

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Oxidative stress has been shown to underlie neuropathological aspects of Alzheimer's disease (AD). 4-Hydroxy-2-nonenal (HNE) is a highly reactive product of lipid peroxidation of unsaturated lipids. HNE-induced oxidative toxicity is a well-described model of oxidative stress-induced neurodegeneration. GSH plays a key role in antioxidant defense, and HNE exposure causes an initial depletion of GSH that leads to gradual toxic accumulation of reactive oxygen species. In the current study, we investigated whether pre-treatment of cortical neurons with acetyl-L-carnitine (ALCAR) and α-lipoic acid (LA) plays a protective role in cortical neuronal cells against HNE-mediated oxidative stress and neurotoxicity. Decreased cell survival of neurons treated with HNE correlated with increased protein oxidation (protein carbonyl, 3-nitrotyrosine) and lipid peroxidation (HNE) accumulation. Pretreatment of primary cortical neuronal cultures with ALCAR and LA significantly attenuated HNE-induced cytotoxicity, protein oxidation, lipid peroxidation and apoptosis in a dosedependent manner. Additionally, pretreatment of ALCAR and LA also led to elevated cellular GSH and heat shock proteins (HSPs) levels compared to untreated control cells. We have also determined that pretreatment of neurons with ALCAR and LA leads to the activation of phosphoinositol-3 kinase (PI3K), PKG and ERK1/2 pathways, which play essential roles in neuronal cell survival. Thus, this study demonstrates a cross talk between the PI3K, PKG and ERK1/2 pathways in cortical neuronal cultures that contributes to ALCAR and LA-mediated pro-survival signaling mechanisms. This evidence supports the pharmacological potential of co-treatment of ALCAR and LA in the management of neurodegenerative disorders associated with HNE-induced oxidative stress and neurotoxicity, including AD.

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Nitric oxide synthase induction in astroglial cell cultures: Effect on heat shock protein 70 synthesis and oxidant/antioxidant balance

et al. 2000

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Glial cells in the nervous system can produce nitric oxide in response to cytokines. This production is mediated by the inducible isoform of nitric oxide synthase. Radical oxygen species (ROS) and nitric oxide (NO) derivatives have been claimed to play a crucial role in many different processes, both physiological such as neuromodulation, synaptic plasticity, response to glutamate, and pathological such as ischemia and various neurodegenerative disorders. In the present study we investigated the effects of NO synthase (iNOS) induction in astrocyte cultures on the synthesis of heat shock proteins, the activity of respiratory chain complexes and the oxidant/antioxidant balance. Treatment of astrocyte cultures for 18 hr with LPS and INFgamma produced a dose dependent increase of iNOS associated with an increased synthesis of hsp70 stress proteins. This effect was abolished by the NO synthase inhibitor L-NMMA and significantly decreased by addition of SOD/CAT in the medium. Time course experiments showed that iNOS induced protein expression increased significantly by 2 hr after treatment with LPS and INFgamma and reached a plateau at 18 hr; hsp70 protein synthesis peaked around 18 and 36 hr after the same treatment. Addition to astrocytes of the NO donor sodium nitroprusside resulted in a dose dependent increase in hsp70 protein that was comparable to that found after a mild heat shock. Additionally, a decrease in cytochrome oxidase activity, a marked decrease in ATP and protein sulfhydryl contents, an increase in the activity of the antioxidant enzymes mt-SOD and catalase were found which were abolished by L-NMMA. These findings suggest the importance of mitochondrial energy impairment as a critical determinant of the susceptibility of astrocytes to neurotoxic processes and point to a possible pivotal role of hsp70 in the signalling pathways of stress tolerance.

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Stress Proteins and SH-Groups in Oxidant-Induced Cellular Injury After Chronic Ethanol Administration in Rat

Cited by 91 publications

References 39 publications

Alcohol stress, membranes, and chaperones

Alcohol stress, membranes, and chaperones

Involvement of PI3K/PKG/ERK1/2 signaling pathways in cortical neurons to trigger protection by cotreatment of acetyl-L-carnitine and α-lipoic acid against HNE-mediated oxidative stress and neurotoxicity: Implications for Alzheimer's disease

Nitric oxide synthase induction in astroglial cell cultures: Effect on heat shock protein 70 synthesis and oxidant/antioxidant balance

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