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1. Maternal intake of 1 mEq CsCl in drinking water at conception until weaning the offspring mice resulted in certain maternal mediated neonatal and developmental toxicity. 2. Initial reduction in body and brain weights were determined in male offspring due to maternal exposure to Cs salt before they attained the control levels. 3. Offspring from both sexes showed increased spleen weight from control as a consequence of maternal exposure to Cs. This may precipitate delayed immunotoxicity. 4. Maternal Cs exposure did not alter litter size or specific activities of offspring heart lactate dehydrogenase isoenzymes from respective controls. 5. Maternal exposure to Cs altered specific activities of offspring liver alcohol- and aldehyde dehydrogenase during development compared to controls. 6. The results indicate neonatal and developmental toxicity of Cs as a function of maternal intake of CsCl during pregnancy and breast feeding.

1. A brief overview of gonadal alcohol dehydrogenase (ADH) and aldehyde-dehydrogenase (ALDH) is presented and their relationships to gonadal toxicity of ethanol has been discussed. 2. The distributions of ADH and ALDH among major reproductive tissues of rodents, their subcellular localization and kinetic properties were summarized. 3. The sensitivity of testicular ADH and ALDH to ethanol intake, various psychoactive agents and steroidal compounds was assessed and the implication of these enzymes in gonadal ethanol-drug interaction has been suggested. 4. The possible role of testicular ALDH in tumorigenesis and in high altitude endocrine sensitivity to ethanol has been addressed.

1. Breast fed maternally-mediated developmental LiCl toxicity was determined in mice offspring as a function of offspring's gender and duration of maternal intake of LiCl (1 mEq). 2. The female offspring were more sensitive than the males to major organ weight changes by maternal exposure to LiCl. 3. Maternal intake of LiCl from preconception until weaning of the nurslings induced offspring hepatic alcohol dehydrogenase and heart lactate dehydrogenase in both sexes which was isoenzyme specific for the latter. 4. The offspring also showed induction of liver aldehyde dehydrogenase but only as consequences of postnatal exposure to LiCl. 5. The results indicate offspring developmental toxicity as a consequence of maternal exposure to Li salts and breast feeding.

1. Gossypol, an antifertility ingredient of the cotton plant, altered specific activity of mouse liver alcohol dehydrogenase (L-ADH) and subcellular aldehyde dehydrogenase (L-ALDH) in mice of both sexes. 2. Intraperitoneal injection of a single gossypol dose, 50 mg/kg, inhibited both male and female L-ADH and cytoplasmic L-ALDH from saline controls 21 hr after drug treatment. 3. Gossypol inhibited female but not male mouse mitochondrial L-ALDH isoenzymes. 4. Gossypol-produced enzyme inhibition was determined as noncompetitive. 5. The results suggest gender-dependent sensitivity of mitochondrial L-ALDH to the gossypol inhibition. A toxic metabolic interaction between ethanol and gossypol has been indicated which suggests the contraindication of alcoholic beverages during gossypol use.

1. The effect of beta-endorphin (beta-EP) and morphine sulfate (MS), in presence and absence of naloxone (NX), on chicken chorioallantoic membrane was studied as a function of blood vessel proliferation. 2. A 50% reduction in blood vessel proliferation occurred by 10 micrograms of beta-EP or by 5 micrograms of MS per egg compared to controls. 3. An individual dose, i.e. 5 micrograms of beta-EP, did not significantly inhibit blood vessel counts after initial 24 hr period of the drug application when given alone compared to inhibition occurring with combined use of NX. 4. NX (1 microgram) did not significantly reverse the angiostatic effects of MS (10 micrograms) or of beta-EP (5 micrograms). 5. The observed modulation of angiogenesis by opioids suggests involvement of beta-EP and MS in the proliferation of vascular endothelial cells. 6. This may be due to an effect of beta-EP and MS on cell-mediated immunity factors such as interferons, interleukins and prostaglandin E2.

1. Equal dose regimens of amitriptyline, a tertiary amine tricyclic antidepressant, were more potent than nortriptyline, a secondary amine derivative, in suppressing CDF-1 mouse locomotor activity. 2. A suggestive increase in dopamine turnover rate in mouse cerebral cortex and striatal brain regions was apparent by amitriptyline but not nortriptyline. 3. A suggestive increase in serotonin turnover in mouse cerebellum and striatum was determined for nortriptyline. 4. Both antidepressants increased cerebral cortex, midbrain and cerebellum serotonin levels from saline control. 5. Increases of regional brain dopamine by amitriptyline and serotonin by nortriptyline concurrent with reuptake blockade of the respective serotonin and dopamine may contribute to their differential extrapyramidal and sedating side effects.

1. Short-term treatment with tamoxifen (a nonsteroidal antiestrogen) decreased mouse spontaneous locomotor activity compared to controls. 2. Short-term pretreatment with tamoxifen prior to an acute sedative dose of ethanol potentiated ethanol-medicated behavioral depression in the mouse. 3. Injection of a small dose of Leu-enkephalin, which is devoid of effect on mouse motility, prior to an acute sedative dose of ethanol to tamoxifen pretreated female mice counteracted ethanol-produced suppression of motor activity. 4. Mouse liver aldehyde dehydrogenase was inhibited by the short-term administration of tamoxifen when given alone or preceding acute dosages of Leu-enkephalin. Concomitantly, there was an increase in blood plasma ethanol concentration from corresponding control. 5. The results of the behavioral performance test used suggest that tamoxifen possesses depressant property and exerts synergestic effect with Leu-enkephalin in antagonizing ethanol-produced behavioral depression in the mouse. 6. The enzymatic part of the study indicates an adverse metabolic influence by tamoxifen on hepatic metabolism of ethanol-derived acetaldehyde which could contribute to the potentiation of the sedative effect of ethanol.

1. Spontaneous locomotor activity of four mouse strains, the albino ICR, BALB/C, the black C57 BL/6 and the brown CDF-I, was studied in conjunction with whole brain content of select biogenic amines and major metabolites. The ICR and C57BL/6 mice scored the highest and lowest motility among the strains studied, respectively. 2. The ICR mice motility were the most sensitive to experimental stress among the mouse strains evaluated. 3. Brain dopamine concentrations were greater in ICR and CDF-I mice than the other two mouse strains. This is compared to high serotonin and 5-hydroxyindole acetic acid levels determined in C57BL/6. 4. A relationship between the ICR mouse strain with a high motility and the ratios of brain dopamine:homovanillic acid and between serotonin:5-hydroxyindole acetic acid was established. 5. An inverse relationship between ICR mice motility and the ratio of metanephrine and normetanephrine:3-methoxy-4-hydroxyphenylglycol (MHPG) was determined. 6. It is concluded that genetic predisposition may account for a relationship between motor activity and brain biogenic amines which may give insight into the susceptibility of different patients to the development of certain extrapyramidal diseases.

1. Female rats were placed on water, 5% ethanol (ET), or 20% ET drinking solutions for 8 weeks. The last 2 weeks, the rats received orally either ethinyl estradiol (EE), norethindrone acetete (NED), or a combination of both. 2. Luteinizing hormone decreased due to ET drinking and was undetectable subsequent to the steroidal treatment. 3. Prolactin increased after steroid treatment and alcohol drinking in the controls. 4. Ethanol (5%) plus EE increased prolactin as did the steroidal combination, whereas ET (20%) likewise increased prolactin in conjunction with NED over water controls. 5. Hepatic alcohol dehydrogenase was inhibited due to EE when compared to water-controls in the 5% ET drinking animal, whereas aldehyde dehydrogenase was induced in combination with NED in both the 5% and 20% ET drinking rats.