Effect of ethanol on turpentine-induced acute phase response in rats

Nadkarni, G.D.; Pestonjamasp, Kersi

doi:10.1016/0006-2952(85)90184-4

Cited by 6 publications

(4 citation statements)

References 12 publications

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“…However, one study does indicate that the rate of synthesis of acute phase proteins, but not the concentration of these proteins in blood is suppressed by ethanol in a rat model using turpentine to induce the acute phase response (Nadkarni & Pestonjamasp 1985). These results are difficult to compare with the results in the present study because none of the same acute phase proteins were examined in the two studies.…”

Section: Discussioncontrasting

confidence: 86%

An explanation for the paradoxical induction and suppression of an acute phase response by ethanol

Pruett

2006

Alcohol

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Binge ethanol (EtOH) consumption suppresses inflammatory responses and resistance to infection, but paradoxically it is associated with increased levels of acute phase proteins (which are indicators of inflammation) and an increased risk of inflammation mediated pathologies such as cardiovascular disease and cirrhosis of the liver. The latter effect may be mediated by increased translocation of bacteria leading to activation of toll-like receptor 4 (TLR4). In this study, the dose-response and time course of the effects of EtOH alone or EtOH in conjunction with a TLR 4 agonist (LPS) were evaluated in mice. Ethanol alone at a dosage of 6 g/kg induced an acute phase response (as indicated by ELISA for serum amyloid A and serum amyloid P) that was maximal 24 hr after dosing. Lower dosages of EtOH did not have this effect but did suppressed the acute phase response to LPS and the production of IL-6 up to 3 hr after dosing. EtOH at 6 g/kg did not induce an acute phase response in C3H/HeJ (TLR4 mutant) mice, indicating that this response is mediated through TLR4. These results provide a resolution for the apparently paradoxical pro-and anti-inflammatory actions of EtOH with regard to acute phase responses.

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Section: Discussioncontrasting

confidence: 86%

An explanation for the paradoxical induction and suppression of an acute phase response by ethanol

Pruett

2006

Alcohol

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“…This is in accordance with albumin's role as a so‐called negative acute‐phase protein that decreases with the increased acute‐phase demand for liver export proteins. Our findings are consistent with an earlier rat study that showed that acute EtOH exposure inhibited the turpentine‐induced increase in the rate of acute‐phase protein synthesis and enhanced the negative effects of turpentine on the rate of albumin synthesis (Nadkarni and Pestonjamasp, ). Our results are also consistent with the aforementioned mice study, which further showed that acute EtOH exposure suppressed the LPS‐induced acute‐phase protein response (Pruett and Pruett, ).…”

Section: Discussionsupporting

confidence: 93%

“…These proteins promote the clearance of invading pathogens, modulate the immune response against them, and help to restore the disturbed homeostasis (Fey and Gauldie, ; Gabay and Kushner, ), thus underlining acute‐phase protein synthesis as a critically important liver function. A few studies have investigated the effects of acute ethanol (EtOH) exposure on an experimentally induced acute‐phase response in animals (Nadkarni and Pestonjamasp, ; Pruett and Pruett, ), and in these studies, an impaired acute‐phase response was found. However, no previous study has investigated how long‐term EtOH exposure affects the hepatic acute‐phase response to endotoxin in rats; this was the aim of our study.…”

mentioning

confidence: 99%

Long-Term Ethanol Exposure Decreases the Endotoxin-Induced Hepatic Acute Phase Response in Rats

Glavind

Vilstrup

Grønbæk

et al. 2017

Alcohol Clin Exp Res

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“…These associated conditions may act either in concert or antagonistically with respect to total hepatic protein synthesis, plasma protein synthesis and expression of RNA genes. While inflammation may stimulate overall hepatic protein synthesis (Schreiberg et al, 1982;Nadkarni and Pestonjamasp, 1985), food deprivation is inhibitory (McNurlan et al, 1979;Garlick et al, 1975). The liver in a TB host is thus under the influence of several factors simultaneously.…”

mentioning

confidence: 99%

RNA polymerase activity and protein synthesis in mouse tumor‐host liver compared to benign para‐neoplastic reactions

Ternell

Zachrisson

Lundholm

1988

Intl Journal of Cancer

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Elevated protein synthesis in mouse tumor-host liver is the net result of both stimulatory and inhibitory responses. This study compares the directional change in transcription and synthesis of liver and plasma proteins in tumor-host liver as compared with para-neoplastic conditions, such as malnutrition, inflammation, benign cell proliferation and protein deficiency. A methylcholanthrene-induced sarcoma was used in weight stable mice (C57BI/6J). Inflammation was induced by s.c. turpentine injection, and benign cell proliferation by injection of heat-killed Corynebacterium parvum. DNA-dependent RNA-polymerase activity (I, II and III) (EC2.7.7.6) was measured in isolated hepatic nuclei. Protein synthesis was measured by labelling of hepatic and plasma proteins following the injection of a "flooding dose" of the labelled amino acid. Benign hepatic cell proliferation and sterile inflammation caused increased rates of transcription, while malnourished and healthy control animals had lower hepatic transcription than animals bearing a malignant tumor. Inflammation was associated with increased activities of free (nonchromatin engaged) RNA polymerase, which was not found in any other para-neoplastic condition or in the tumor-host liver. A protein- and calorie-deficient state was associated with depressed hepatic and plasma protein synthesis compared with the tumor condition. Tumor-host livers had a nonsecretory protein synthesis rate equal to that of normal livers, but 45% higher plasma protein synthesis. Animals with inflammation and benign cell growth had liver protein synthesis rates which were approximately 50% higher than in tumor-bearing animals, but plasma protein synthesis in tumor-bearing animals was comparable with that of animals which had inflammation. Benign cell growth was not associated with an overall elevated plasma protein synthesis. The translation rate per transcription activity was highest in normal animals and decreased in animals suffering from either tumor, protein deficiency or benign cell proliferation. Hepatic protein synthesis in tumor-host livers is high considering the degree of anorexia and malnutrition, although not as high as in livers from animals with pronounced inflammation. This counter-regulation in tumor-host livers may indicate a compensatory state to maintain protein synthesis against attenuating factors such as the declining food intake. Protein metabolism in tumor-host livers represents an unusual combination of findings.

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Effect of ethanol on turpentine-induced acute phase response in rats

Cited by 6 publications

References 12 publications

An explanation for the paradoxical induction and suppression of an acute phase response by ethanol

An explanation for the paradoxical induction and suppression of an acute phase response by ethanol

Long-Term Ethanol Exposure Decreases the Endotoxin-Induced Hepatic Acute Phase Response in Rats

RNA polymerase activity and protein synthesis in mouse tumor‐host liver compared to benign para‐neoplastic reactions

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