Acetaldehyde, the first metabolite of ethanol, has been implicated in the pathogenesis of alcoholic liver disease. In order to investigate a possible immunologic mechanism whereby acetaldehyde might exert its toxic effect acetaldehyde protein conjuates were prepared and characterized. This study demonstrates that acetaldehyde conjugated albumin can be an immunogen, can form a more negatively charged, more acidic, heterogeneous conjugate than albumin and can elicitate a specific rabbit antibody. ELISA can be used to assay antibodies produced in response to acetaldehyde albumin conjugates suggesting that chronic alcohol ingestion can lead the generation of antibodies against acetaldehyde conjugated human serum albumin. The significance of this study is that it possibly can provide a method to investigate the mechanism responsible for the sequelae of alcoholism.

The possible significance of cognitive and situational factors in determining the response to alcohol suggests that behavioral changes following drinking may reflect a lack of self-control not solely attributable to the pharmacological effect. In an initial experiment subjects were requested to overcome the effects of alcohol (1.32 ml/kg 95% ethanol). In comparison with a no-motivation group (n = 11), motivated subjects (n = 14) demonstrated compensation on aspects of tasks involving memory, coordination and affect. It was speculated that attributions of causality (internal or external) for relative control might influence its occurrence and maintenance. In a second experiment false dose feedback was expected to interact with relative control to affect subjects' (n = 45) attributions. A greater level of sobriety was achieved by subjects who were led to attribute responsibility to themselves. Also, it appeared that further drinking was affected by cognitive influences. Implications of the self-control phenomenon, especially regarding the non-pharmacological role and the etiology of excessive drinking, are discussed.

The neuroanatomical consequences of chronic ethanol ingestion were investigated using neuropsychological tests selectively sensitive to damage in circumscribed brain areas-~~~ The performance of a group of male alcoholics (N=15) with a self-reporte?- drinking history less than ten years, and a group of male alcoholics (N=15) with a self-reported drinking history of ten or more years was compared to a group of male nqnalcoholic controls (N=15). l.A--multiple covariate analysis was done prior to analyzing group differences to determine what influence three covariates (age, education and socioeconomic status) had on the group performances. Results from this analysis indicated that some of the tests were significantly influenced by age or education but no significant Group x Covariate interactions were observed. /JCn agreement with numerous neuropathological findings, the late stage alcoholics were found to be principally deteriorated on the tests of frontal lobe functioning, followed by lesser impairment on the tests of temporal lobe functioning, with no evidence of impairment on the tests of parietal lobe functioning~ No significant group differences were found betv1een the early stage alcoholics and the controls~ Small but negative correlations were found between both the duration of alcoholism and the average amount of alcohol consumed with each of the neuropsychological measures given in this study.

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This research was designed to study the perinatal and postweaning effects of the interaction between ethanol and low dietary zinc during gestation and lactation in the rat. Pregnant rats were fed liquid diets containing either 2 or 10 μg zinc/ml with or without 30% of kcal from ethanol throughout gestation and lactation. The liquid diet formulation was nutritionally adequate to insure offspring growth and survival during lactation. At weaning, dams and five of eight offspring from each litter were killed by exsanguination under sodium pentobarbital anesthesia. The remaining offspring were orally inoculated with Streptococcus mutans and fed a caries-promoting diet for six weeks. The low zinc diet produced a moderate zinc deficiency in dams as evidenced by a decrease in tissue zinc content, serum alkaline phosphatase activity, and urinary zinc concentration. Despite the presence of high zinc content in the diet, ethanol antagonized maternal zinc status to a level typical of that produced by the low zinc diet. The lowest zinc status, however, was found when low dietary zinc and ethanol were combined. The maternal interaction between ethanol and zinc also depressed offspring serum zinc and alkaline phosphatase activity in a similar manner but the magnitude was smaller. The maintenance of a lower than normal maternal tissue zinc and decreased maternal urinary excretion of zinc suggested a maternal attempt to support the growth and development of offspring despite zinc deficiency. Physiological consequences of ethanol-antagonized zinc status were evidenced by depressed activity of maternal and offspring serum alkaline phosphatase, increased maternal urinary excretion of hydroxyproline, decreased offspring molar enamel and dentin zinc content, increased dental caries score, and decreased cross-linking structure of mandibular second molar enamel. The liquid diet developed in the present study was nutritionally adequate and allowed for the investigation of a single nutrient deficiency, zinc, in ethanol fed rats during gestation and lactation without confounding effects of general malnutrition. Although the direction of interaction was predominately an effect of ethanol on zinc rather than the effect of zinc on ethanol, this study clearly indicates that zinc deficiency is an important consequence of maternal ethanol ingestion. / Graduation date: 1984

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