Peptidase activities of the multicatalytic protease in rat liver after voluntary and intragastric ethanol administration

Donohue, Terrence M.; Zetterman, Rowen K.; Zhang‐Gouillon, Zhi‐Qi; French, Samuel W.

doi:10.1002/hep.510280228

Cited by 69 publications

(61 citation statements)

References 45 publications

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“…acetaldehyde and malondialdehyde-acetaldehyde) [34] derived from ethanol metabolism may impair autophagy, similar to that which occurs with the proteasome [35][36][37] . Some of the current evidence for this is circumstantial, but nevertheless compelling as there is evidence of lysosomal damage, as judged by enhanced lysosomal fragility, which could result from either altered lipid metabolism, oxidative stress or both [15] .…”

Section: Suppression Of Autophagymentioning

confidence: 99%

Autophagy and ethanol-induced liver injury

Donohue¹

2009

WJG

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The majority of ethanol metabolism occurs in the liver. Consequently, this organ sustains the greatest damage from ethanol abuse. Ethanol consumption disturbs the delicate balance of protein homeostasis in the liver, causing intracellular protein accumulation due to a disruption of hepatic protein catabolism. Evidence indicates that ethanol or its metabolism impairs trafficking events in the liver, including the process of macroautophagy, which is the engulfment and degradation of cytoplasmic constituents by the lysosomal system. Autophagy is an essential, ongoing cellular process that is highly regulated by nutrients, endocrine factors and signaling pathways. A great number of the genes and gene products that govern the autophagic response have been characterized and the major metabolic and signaling pathways that activate or suppress autophagy have been identified. This review describes the process of autophagy, its regulation and the possible mechanisms by which ethanol disrupts the process of autophagic degradation. The implications of autophagic suppression are discussed in relation to the pathogenesis of alcohol-induced liver injury.

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Section: Suppression Of Autophagymentioning

confidence: 99%

Autophagy and ethanol-induced liver injury

Donohue¹

2009

WJG

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“…Ethanol consumption slows down the rate of hepatic protein catabolism. Such changes may be related to the degree of ethanol-induced oxidative stress (28).…”

Section: Albumin and Globulinmentioning

confidence: 99%

Biochemical markers for alcohol consumption

Das

Nayak

Vasudevan

2003

Indian J Clin Biochem

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A variety of laboratory tests are available to assist in the diagnosis of alcohol consumption and related disorders. The levels of intake at which laboratory results become abnormal vary from person to person. Laboratory tests are particularly useful in settings where cooperativeness is suspected orwhen a history is not available. Several biochemical and hematological tests, such as T-glutamyltransferase (GGT) activity, aspartate aminotransferase (AST) activity, highdensity lipoprotein cholesterol (HDL-C) content of serum, and erythrocyte mean corpuscular volume (MCV) are established markers of alcohol intake. Their validity as markers is based largely on correlations with recent intake at a single time point and on decreases in elevated values when heavy drinkers abstain from alcohol. These readily available laboratory tests provide important prognostic information and should be integral part of the assessment of persons with hazardous alcohol consumption. There are several other markers with considerable potential for more accurate reflection of recent alcohol intake. These include carbohydrate deficient transferrin, ~-hexosaminidase, acetaldehyde adducts and the urinary ratio of serotonin metabolites, 5-hydroxytryptophol and 5-hydroxyindoleacetic acid. These markers provide hope for more sensitive and s.pecific aids to diagnosis and improved monitoring for intake.

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“…Processing of protein antigens within inducible subunits of IPR is important in subsequent conjugation with the class I major histocompatibility complex (MHC) required for antigen presentation [21,23]. While no data are available to suggest that alcohol affects PR function in antigen presenting cells (APC), studies performed using liver cells point to PR impairment as a result of exposure to EtOH or its metabolites [24].…”

Section: Introductionmentioning

confidence: 99%

Alcohol and HIV decrease proteasome and immunoproteasome function in macrophages: implications for impaired immune function during disease

Haorah

Heilman

Diekmann

et al. 2004

Cellular Immunology

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Proteasomes (proteinase complexes, PR) and immunoproteasomes (IPR) degrade damaged proteins and affect protein processing required for antigen presentation by mononuclear phagocytes. These critical immune processes are attenuated during progressive HIV-1 infection and are affected by alcohol abuse. To investigate the mechanisms underlying these functional changes, we measured PR and CYP2E1 activities [an ethanol (EtOH) metabolizing enzyme] and reactive oxygen species (ROS) in human monocyte-derived macrophages (MDM) following HIV-1 infection and EtOH treatment. We observed progressive declines of PR activity and PR/IPR contents in HIV-1-infected MDM. PR activity and IPR expression increased after IFN-c stimulation but reduced after HIV-1 infection. EtOH inhibited both IFN-c-induced PR and IPR. Paradoxically, EtOH attenuated PR catalytic activity in infected MDM and suppressed viral replication. Elevated ROS followed EtOH exposure and paralleled decreased PR activity. The latter was restored by anti-oxidant. The data support the notion that HIV-1 infection and EtOH may work in concert to affect immune function including antigen presentation and thereby affect disease progression.

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Peptidase activities of the multicatalytic protease in rat liver after voluntary and intragastric ethanol administration

Cited by 69 publications

References 45 publications

Autophagy and ethanol-induced liver injury

Autophagy and ethanol-induced liver injury

Biochemical markers for alcohol consumption

Alcohol and HIV decrease proteasome and immunoproteasome function in macrophages: implications for impaired immune function during disease

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