Effects Of Moderate Ethanol Consumption Research Articles

Myocardial mechanical, biochemical, and structural alterations induced by chronic ethanol ingestion in rats.

To determine the effects of moderate ethanol consumption on the mechanical, biochemical, and structural characteristics of the heart, myocardial mechanical performance, contractile protein enzyme activity, and the number and size of myocytes were measured in male Fischer 344 rats after the ingestion of 30% oral ethanol. Papillary muscles removed from the left ventricle were greater in length, weight, and cross-sectional area than the corresponding muscles from the right side. However, no differences were found between control and ethanol-treated myocardium when either the left or right side was compared separately. Chronic ethanol ingestion resulted in an increase in resting tension in left ventricular muscles, with no alteration in peak developed tension. Moreover, time to peak tension was significantly prolonged, whereas a depression was observed in the peak rate of isometric tension development. Isotonically, left muscles from ethanol-treated rats revealed a prolongation of time to peak shortening and a marked depression in the velocity of shortening at physiological loads. No changes were noted in muscles from the right ventricle. Contractile protein enzyme activity revealed no differences in myofibrillar Mg(2+)-ATPase activity in right and left ventricular myocardium between control and ethanol-treated rats in the presence of EGTA. However, at physiological activating levels of calcium, an upward shift of the myofibrillar Mg(2+)-ATPase activity-calcium curve occurred in left myocardium, whereas a depression in this relation was seen in the right ventricle. As a result of chronic ethanol intake, a decrease was noted in the volume percent of myocardium occupied by myocytes, and that myocyte cell volume per nucleus was found to remain essentially constant throughout the various layers of the ventricular wall. Importantly, a 14% significant decrease in the total number of myocyte nuclei was demonstrated in the left ventricular myocardium of rats on chronic ethanol consumption. Thus, chronic but moderate alcohol ingestion resulted in depressed contractile performance, alterations in myofibrillar Mg(2+)-ATPase activity, and myocyte loss. These events may serve to function as preliminary indicators of the onset of heart failure of alcoholic origin in this animal model.

Effect of moderate ethanol consumption on mammary gland structural development and DNA synthesis in the female rat

Epidemiological and experimental evidence provides support for a positive association between alcohol consumption and the development of breast cancer. To examine a mechanism for this association, young female Sprague-Dawley rats were pair-fed liquid diets containing ethanol at 0%, 15%, 20%, and 25% of calories for 32 days. The structural development and DNA-labeling index of the mammary gland were determined. Ethanol consumption at 20% and 25% of calories increased the density of carcinogen-sensitive terminal end bud (TEB) structures and decreased the density of carcinogen-insensitive alveolar bud structures of the developing mammary gland as compared to ad lib-fed and pair-fed controls. Consumption of ethanol at 20% and 25% of calories was also associated with a significant enhancement in the DNA-labeling index of mammary gland TEB structures, the target tissue for chemically-induced rat mammary tumorigenesis. In a separate study, serum progesterone but not estradiol, was decreased for rats fed ethanol at 25% of calories as compared to ad lib-fed and pair-fed controls. Thus moderate ethanol consumption at 20% and 25% of calories can delay the maturation and increase TEB DNA synthesis of the normal rat mammary gland. These changes may be explained by an ethanol-associated decrease in serum progesterone, a hormone important for the maturation of the mammary gland epithelium in the young female rat.

Ethanol administration does not alter dopamine D 1 and D 2 receptor characteristics in rat brain

The effects of 5 weeks' ethanol treatment on the number and affinity of cortical and striatal dopamine D 1 receptors and striatal D 2 receptors in rat brain were investigated. The ethanol and control diets were carried out using the pair-feeding technique. The number and affinity of dopamine D 1 receptor sites in the frontal cortex and caudate-putamen or D 2 receptors in the caudate-putamen were not significantly altered by the used ethanol dose regimen. This study demonstrates that if dietary factors related to ethanol consumption are carefully controlled no ‘specific’ ethanol-induced changes in striatal D 1 and D 2 or cortical D 1 receptor characteristics can be observed after 5 weeks' ethanol consumption. Thus, changes in the central dopamine receptors are not likely to play any significant role in the effects of moderate ethanol consumption on neuronal function.

Metabolic effects of acetaldehyde.

Acetaldehyde, the toxic product of ethanol metabolism in the liver, covalently binds to a variety of proteins, thereby altering liver function and structure. Through its binding to tubulin, acetaldehyde decreases the polymerization of microtubules thereby impairing protein secretion and favouring their retention, with associated swelling of hepatocytes. Acetaldehyde adduct formation also impairs some enzyme activities. Either directly or through binding with GSH, acetaldehyde favours lipid peroxidation. Various mitochondrial functions are altered, particularly after chronic ethanol consumption which sensitizes the mitochondria to the toxic effects of acetaldehyde. In cultured myofibroblasts, acetaldehyde stimulates collagen production. The acetaldehyde-protein adducts stimulate the production of antibodies directed against the acetaldehyde epitope. This immune response may contribute to the aggravation or perpetuation of alcohol-induced liver damage. Some acetaldehyde effects, however, could conceivably be considered as beneficial, such as the stimulation of vascular prostacyclin release which may take part in the 'protective' effect of moderate ethanol consumption against some cardiovascular complications.

Experimental basis of standardized specimen collection: The effect of moderate ethanol consumption on some serum components (K, Na, ASAT, ALAT, CK, LD, total protein)

Experimental basis of standardized specimen collection: The effect of moderate ethanol consumption on some serum components (K, Na, ASAT, ALAT, CK, LD, total protein)

Experimental basis of standardized specimen collection: the effect of moderate ethanol consumption on some serum components (K, Na, ASAT, ALAT, CK, LD, total protein).

Venous blood was collected on two mornings from seven healthy volunteers using the standard Scandinavian procedure (fasting, sitting and no tourniquet) and serum Na, K, ASAT, ALAT, CK, LD and total protein were assayed. Then ethanol (0.75 g/kg body weight) was given on three consecutive evenings and the subsequent observed values 1, 3, 15, 38, 62 and 110 h post-ethanol were compared with the morning values. The mean component/total protein ratios dropped 14% for ASAT and 19% for ALAT 62 and 15 h post-ethanol, respectively. CK rose 17% at 3 h and dropped 17% at 62 h. However, the absolute values of ASAT, ALAT and CK did not change significantly. The only significant post-ethanol changes occurred in Na +2.14 mmol/l at 1 h (p less than 0.01), K -0.24 mmol/l at 3 h (p less than 0.05) and +0.26 mmol/l at 15 h (p less than 0.05), and LD +31 IU/l at 15 h (p less than 0.05) and +25 IU/l at 110 h (p less than 0.01). In one series, the total protein concentration dropped 4.57 g/l at 110 h post ethanol (p less than 0.001) but this drop was not reproducible in two additional series. It is concluded that moderate (social) ethanol consumption does not produce clinically significant effects on the components analysed. Also it may be misleading to express results as component/total protein ratios.

Combined effects of moderate ethanol consumption and a low-protein diet during gestation on brain development in [formula omitted] mice

We investigated whether or not moderate ethanol consumption during gestation would interact with the effects of a low-protein diet in affecting brain development in BALB c mice. The independent variables included fetal body and brain weights and cross-sectional area in midsagittal sections of the corpus callosum (CC) and anterior commissure (CA). Pregnant animals were fed either ethanol 12% v/v or an isocaloric sucrose solution from days 5 to 19 of gestation, when fetal development was assessed. In addition, the animals were fed semisynthetic isocaloric diets containing either 8 or 20% casein. All animals were pair-fed to those in the group receiving ethanol and 20% casein; an additional control group was fed lab chow ad libitum. There was clearly an interactive effect of diet and ethanol consumption on blood alcohol concentrations: those in the low-protein group were significantly higher than in the normal-protein group. Similarly, the effect on body weight in the group receiving low protein plus ethanol was greater than the additive effect of either treatment alone, although this may have been due partly to differences in litter size. Brain weight in this group was also significantly less than in the other three groups, which did not differ from each other. Covariance analysis, adjusting brain weight for body weight, suggested a brain-sparing effect of low protein but not ethanol. Neither treatment affected the incidence of the CC being absent at midline. The low-protein treatment decreased the cross-sectional area of both the CC and CA; the effect on the CC was independent of brain weight. There was no effect of ethanol on either of those measures.