摘要:

The aldehyde dehydrogenase (ALDH; EC 1.2.1.3) activity was determined in samples of whole blood and in isolated erythrocytes and leukocytes from users of Swedish moist snuff, cigarette smokers and non‐tobacco‐using controls. The mean whole blood ALDH activity of the smokers was reduced by 21% (P<0.001) when compared to the controls, while that of the snuff users was reduced by only 8% (not significant). Similar but somewhat less pronounced differences were obtained both in the assays with erythrocytes and leukocytes. In the cigarette smokers, the whole blood activity correlated significantly (r= ‐0.79, P<0.001) with the plasma concentration of cotinine, the major metabolite of nicotine, whereas no correlation was observed for the users of moist snuff. Similar plasma nicotine and cotinine levels were found in smokers and snuff users, which indicates that the reduced blood ALDH activity in smokers is not caused by nicotine or any of its metabolites, but more likely, by components formed during combustion of tobacco. Since a reduced blood ALDH activity has previously been suggested as an indicator of excessive alcohol consumption, the present results show that, in future studies on blood ALDH, the smoking habits should also be taken into ac

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1991.tb00510.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1991.tb00511.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

The present study was conducted to determine whether the antisecretory agents colchicine and ethanol affect the intracellular degradation of plasma proteins in rat liver. Plasma proteins were prelabeled in vivo with [3H]leucine and their levels were monitored immunochemically in both the medium and extracts of rat liver slices incubated alone or in the presence of 50 μM colchicine or 25 mM ethanol. Compared with those left untreated, colchicine‐treated slices had a 40‐55% lower secretory capacity and, at one point, showed significant hepatocellular retention of total plasma proteins. Plasma protein secretion by ethanol‐treated liver slices was 22‐32% lower than controls, but there was no detectable retention of unsecreted plasma proteins in the ethanol‐treated liver tissue. In all experiments, the total radioactivity in plasma proteins (i.e., the immunoprecipitable radioactivity in the liver plus that in the medium) decreased with time in a manner suggestive of intracellular degradation. Regression analyses of the rates of degradation of presecretory proteins revealed that compared with controls, plasma protein catabolism was accelerated 57% in colchicine‐treated slices. In ethanol‐treated liver slices, there was a 50% increase in the degradation of total plasma proteins and a 46% increase in albumin catabolism. In all cases, degradation was intracellular. These findings indicate that inhibition of hepatic protein secretion by either colchicine or ethanol is associated with accelerated catabolism of unsecreted plasma proteins, suggesting that hepatocellular degradative processes are responsive to changes in the levels of presecretory proteins and/or perturbations of the sec

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1991.tb00512.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

In 25‐alcohol‐dependent patients in whom detoxication treatment has been introduced serum total β‐hexosaminidase, thermostable β‐hexosaminidase, α‐mannosidase and γ glutamylotransferase (GGT) and serum high density lipoprotein (HDL) cholesterol were determined during alcohol withdrawal. The assays were also performed in a group of dependent individuals after a 1 month or longer period of abstinence. Marked increase in β‐hexosaminidase activity was observed in intoxicated patients. The activity decreased rapidly after the cessation of drinking, resembling the decrease in HDL cholesterol level in its dynamics. The α‐mannosidase activity rise was less pronounced and its normalization was slow, similar to the GGT activity normalization rate. The rise of ã‐hexosaminidase activity was mostly due to the thermostable component of the enzyme. Total β‐hexosaminidase or thermostable β‐hexosaminidase activity determinations appear to be simple and relia

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1991.tb00513.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Effects of 4‐week food restriction and ethanol consumption on natural killer (NK) cell activity and carcass composition were evaluated. Female, C57BL/6 mice given water (H2O) or ethanol (20% w/v, ETOH) ad libitum were placed in one of three dietary groups: unrestricted (UNR), moderately restricted (MR, 2.2 g/day), or severely restricted (SR, 1.8 g/day).Food restriction alone (MR, SR) significantly reduced body, spleen, and thymus weights; carcass lipid content (SR only); spleen cell number; and baseline and interleukin‐2 (rlL‐2) stimulated NK cell activities. Ethanol consumption was unaffected by food restriction and in restricted mice it did not suppress food intake. Thus, average calories derived from ethanol increased from 30% (UNR) to 40% (SR) with the degree of food restriction in these groups. Mice given ethanol and restricted food intake had at least as heavy or heavier body, spleen, and thymus weights than water‐drinking (H2O) counterparts. Spleen cell number was reduced in ethanol‐consuming (ETOH), food restricted groups compared with UNR H2O control. Baseline NK cell activity was suppressed 50% to 90% in all ETOH and food‐restricted groups. rlL‐2 stimulated NK cell activity was suppressed 18% to 76% in food restricted mice independent of ethanol intake. These results indicate that supplementary ethanol calories did not enhance NK cell activity in UNR ETOH mice, nor did they protect splenic NK cell activity from the suppressant effects of food restriction.Ethanol consumption significantly increased carcass lipid content in all groups compared with their H2O counterparts. This increase was largely responsible for the preservation of body weight in ETOH mice especially during food restriction. Therefore, caution must be exercised when using body weight as an indicator of nutritional status

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1991.tb00514.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Major improvement in the homeothermic ability of the rat occurs during the first 2 weeks of postnatal development. Changes in thermoregulatory responsiveness to a single injection of ethanol (EtOH) may occur during this period immature rats (2‐3, 8‐9, and 14‐15 days of age) were administered either saline or EtOH (2 or 4 g/kg BW ip) at thermoneutral ambient temperatures (Ta). In one experiment, metabolic rate (MR) and body temperatures (colonic and skin) were recorded for 1‐3 hr postinjection. A second experiment determined blood EtOH concentration in rats from the 3 age groups over an 8‐hr period following injection of EtOH. 4 g EtOH/kg produced few significant reductions in thermoregulatory function of 2‐3 day‐old rats, but decreased MR by 16% and colonic temperature by 0.5‐0.7OC in 8‐15 day‐old animals. 2 g EtOH/kg had no effect on 8‐9 day‐old rats, but reduced MR and colonic temperature in rats aged 14‐15 days. In every case, the hypothermic response to EtOH was correlated with a reduction in MR. Back and abdominal skin temperatures decreased with colonic temperature, and tail skin temperature indicated EtOH‐induced vasoconstriction in older rats. Blood EtOH concentrations were similar in the three age groups during the first 2 hr postinjection and did not explain differences in metabolic response. The magnitude and duration of thermoregulatory responsiveness to EtOH increases w

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1991.tb00515.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

This study examines the structure of drinking‐related consequences in women in treatment facilities by describing indices that were constructed by submitting 69 measures to factor analysis. Two hundred fifty‐four (254) alcoholic women responded to self‐report interview items that measured the consequences that the respondent perceived to follow or result from her drinking. The items were submitted to a series of exploratory principal component analyses. Nine factors, social withdrawal, sexuality, early effects, maternal role, accidents, symptoms, work, illness, and relationship conflict, emerged in the rotated solution, with the majority of coefficient alphas in the 0.6 to 0.8 range. Internal reliabilities for the indices remained sufficiently high across age subgroups in the s

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1991.tb00516.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Few studies have evaluated the ability of the alcoholic patient to learn treatment‐related information and all have involved conventional educational modalities such as videotape or lecture. Since computer interactive (Cl) programs allow for individualization, feedback, and active learning, we were interested in determining whether Cl would prove to be a more effective educational/treatment modality for male alcoholic patients than the conventional videotape (V) modality. The current study compared the relative effectiveness of the CI and V educational interventions for VA alcoholic patients and a cognitively and sociodemographically matched sample of nonalcoholic VA patients.The 91 male alcoholic subjects (46 V, 45 Cl) were lower socioeconomic outpatients in a VA Alcoholism Treatment program. Control subjects were 35 nonalcoholic men (18 V, 17 Cl) attending an outpatient medical clinic at the same facility. All subjects were individually exposed in a single session to a 1 hr intervention on the Medical Effects of Alcohol. Baseline knowledge was measured prior to the intervention using a 21‐item multiple choice test, while learning and retention were assessed with the same instrument 24 hr after the intervention. All four subgroups (two types of subjects x two types of intervention) identified approximately three more items correctly at the post‐test than at baseline. Thus, neither alcoholics for nonalcoholics acquired more information when exposed to the CI intervention. Further, no differences were found overall in the learning of the alcoholic and nonalcoholic subjects. The implications of these findings and their limitations are disc

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1991.tb00517.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Alcoholic liver disease includes steatosis, alcoholic hepatitis and cirrhosis. Other liver diseases of genetic origin, but with a curious association with alcohol intake, are hemochromatosis and porphyria cutanea tarda. The attribution of chronic hepatitis to alcohol intake remains speculative, and the association may reflect hepatitis C infection. Hepatic injury attributed to alcohol includes the changes reported in the fetal alcohol syndrome.Steatosis, the characteristic consequence of excess alcohol intake, is usually macrovesicular and rarely microvesicular. Acute intrahepatic cholestasis, which in rare instances accompanies steatosis, must be distinguished from other causes of intrahepatic cholestasis (e.g., drug‐induced) and from mechanical obstruction of the intrahepatic bile ducts (e.g., pancreatitis, choledocholithiasis) before being accepted. Alcoholic hepatitis (steatonecrosis) is characterized by a constellation of lesions: steatosis, Mallory bodies (with or without a neutrophilic inflammatory response), megamitochondria, occlusive lesions of terminal hepatic venules, and a lattice‐like pattern of pericellular fibrosis. All these lesions mainly affect zone 3 of the hepatic acinus. Other changes, observed at the ultrastructural level, are of importance in progression of the disease. They include widespread cytoplasmic shedding, and capillarization and defenestration of sinusoids. Progressive fibrosis complicating alcoholic hepatitis eventually leads to cirrhosis that is typically micronodular but can evolve to a mixed or macronodular pattern. Hepatocellular carcinoma occurs in 5 to 15% of patients with alcoholic liver disease.The clinical syndrome of alcoholic liver disease is the result of three factors—parechymal insufficiency, portal hypertension and the clinical consequences of extrahepatic damage produced by alcohol. At the several phases of the life history of alcoholic liver disease, the individual factors play a different role. The clinical manifestations of alcoholic steatosis are mainly extrahepatic in origin. Those of alcoholic hepatitis reflect mainly parenchymal insufficiency and those of cirrhosis are mainly those of portal hypertension.Alcoholic liver injury appears to be generated by the effects of ethanol metabolism and the toxic effects of acetaldehyde, perhaps the immune responses to alcohol‐ or acetaldehyde‐altered proteins, and questionably enhanced by viral hepatitis.Alcoholic hepatitis may be mimicked histologically, and to a varying degree clinically, by a number of conditions (obesity, diabetes, several drug‐induced injuries, jejunoileal bypass, and related “short‐circuiting” of the bowel). Perhaps the most important facet of the hepatotoxicity of alcohol is its enhancement of the effects of a number of other hepatotoxic agents, among which acetaminoph

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1991.tb00518.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

In this prospective study of substance use during pregnancy, women were interviewed in their 4th and 7th prenatal months, and women and children were assessed at 24 hr, 8, 18, and 36 months post‐partum. Data are presented on the outcome of 519 children at age 3. At 3 years, children who were exposed prenatally to alcohol were smaller in weight, length, and head circumference. They also had an increased number of minor physical anomalies. These effects were found even after controlling for nutritional and environmental factors. The persistence of growth effects at age 3 suggests that children exposed to alcohol prenatally may have a diminished capacity for growt

ISSN:0145-6008    

DOI:10.1111/j.1530-0277.1991.tb00519.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY