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Ethanol-induced barrier dysfunction and its prevention by growth factors in human intestinal monolayers: Evidence for oxidative and cytoskeletal mechanisms

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第3期291卷 1075-1085页

作者： Banan, A Choudhary, S Zhang, Y Fields, JZ Keshavarzian, A Rush Univ Med Ctr Dept Internal Med Div Digest Dis Chicago IL 60612 USA

Exposure of intestinal mucosa to ethanol (EtOH) disrupts barrier function and growth factors [epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha)] are protective, but the mechanisms remain obscure. Accordingly, we sought to determine whether the molecular mechanism of EtOH-induced intestinal barrier dysfunction involves oxidative stress and disassembly of microtubules and whether the mechanism of protection by EGF or TGF-alpha involves prevention of these alterations. To this end, human colonic (Caco-2) monolayers were exposed to 0 to 15% EtOH with or without pretreatment with EGF or TGF-alpha (10 ng/ml) or with oxidative or cytoskeletal modulators. Effects on cell viability, barrier function, tubulin (microtubules), and oxidative stress were then determined. Cells were also processed for immunoblots of polymerized tubulin (S2;index of stability) and the monomeric tubulin (S1;index of disruption). EtOH dose-dependently decreased the stable S2 polymerized tubulin and concomitantly increased measures of oxidative stress, including oxidation and nitration of tubulin, fluorescence of dichlorofluorescein, and inducible nitric oxide synthase activity. EtOH also dose-dependently disrupted barrier function and extensively damaged microtubules, and these effects were prevented by pretreatment with antioxidant scavengers: L-cysteine, superoxide dismutase, and L-N-6-1-iminoethyl-lysine (an inducible nitric oxide synthase inhibitor). In monolayers exposed to EtOH, pretreatment with EGF or TGF-alpha prevented the oxidation and nitration of tubulin, increases in the levels of the unstable S1 tubulin, disruption of microtubules, and barrier dysfunction. A microtubule stabilizer (paclitaxel, Taxol) mimicked, in part, the effects of EGF and TGF-alpha, whereas a microtubule disruptive drug (colchicine) prevented the protective effects of these growth factors. We concluded that mucosal barrier dysfunction induced by EtOH involves oxidative stress, which caus

关键词：抗氧化剂/药理学印迹法蛋白质 Caco-2细胞细胞存活/药物作用中枢神经系统抑制药/拮抗剂和抑制剂中枢神经系统抑制药/药理学细胞骨架/药物作用细胞骨架/代谢乙醇/拮抗剂和抑制剂乙醇/药理学荧光抗体技术生长物质/药理学肠黏膜/细胞学肠黏膜/药物作用肠黏膜/代谢显微镜检查共焦微管/药物作用微管/酶学微管/代谢硝酸盐类/代谢一氧化氮合酶/代谢一氧化氮合酶Ⅱ型氧化还原氧化性应激/生理学受体表皮生长因子/免疫学微管蛋白/代谢人类

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Effects of ethanol on working memory and attention in pigeons

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第2期293卷 551-558页

作者： Dayer, CA Baron, S Light, KE Wenger, GR Univ Arkansas Med Sci Dept Pharmacol & Toxicol Little Rock AR 72205 USA Univ Arkansas Med Sci Dept Pharmaceut Sci Little Rock AR 72205 USA

To determine whether the effects of ethanol on working memory are mediated by a secondary effect on attention, dose-response curves for ethanol were determined in eight pigeons trained under a titrating matching-to-sample (TMTS) procedure, in eight pigeons trained under a discrete-trial measure of attention, and in eight pigeons trained under a continuous-trial measure of attention. Ethanol decreased accuracy under the TMTS procedure following the three highest doses (1, 1.8, and 3 g/kg). Only the highest dose (3 mg/kg) decreased rates of responding. Attention, as measured under the discrete-trial procedure, was affected only by the two highest doses (1.8 and 3 g/kg). The 3-g/kg dose caused significant decreases in the probability of a hit and probability of a correct rejection, as well as significant increases in the probability of an error of omission and response latencies. Sensitivity to the signal decreased following 1.8 and 3 g/kg ethanol. Under the continuous-trial procedure, ethanol caused a peak in false alarms after the 1.8-g/kg dose, decreased the probability of a hit following the 1.8- and 3-g/kg doses, and increased probability of a miss at all doses. Sensitivity to the signal was not affected. A comparison of the dose-response curves for the TMTS procedure and the two measures of attention revealed that working memory (TMTS) was decreased by a lower dose than that affecting attention. This suggests that the effects of ethanol on working memory are not mediated by the subject's ability to pay attention to stimulus changes in the environment.

关键词：算法注意力/药物作用中枢神经系统抑制药/血液中枢神经系统抑制药/药理学鸠鸽科条件反射操作式/药物作用剂量效应关系药物乙醇/血液乙醇/药理学记忆短时/药物作用精神运动性行为/药物作用强化分级表信号检测(心理学)/药物作用动物男(雄)性

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Cocaine potentiates ethanol-induced excitation of dopaminergic reward neurons in the ventral tegmental area

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第2期293卷 383-389页

作者： Bunney, EB Appel, SB Brodie, MS Univ Illinois Coll Med Dept Emergency Med MC 724 Chicago IL 60612 USA Univ Illinois Coll Med Dept Physiol & Biophys Chicago IL 60612 USA

The coabuse of cocaine and ethanol is one of the most frequently used substance abuse combinations in the United States. The dopamine (DA) neurons in the ventral tegmental area (VTA) are important in the rewarding mechanism of these two substances. Cocaine is known to block the reuptake of DA and serotonin (5-HT). At concentrations below 1 mu M, cocaine preferentially blocks the reuptake of 5-HT compared with DA. We have previously shown that ethanol increases the firing rate of DA neurons in the VTA, and that this excitation is enhanced by 5-HT. Extracellular single-unit recordings were made from VTA dopaminergic neurons in coronal brain slices from young adult Fischer 344 rats. Cocaine (1-10 mu M) reduced the spontaneous firing rate in VTA dopaminergic neurons in a concentration-related manner. A lower concentration of cocaine (500 nM), which is a concentration that is pharmacologically relevant in addicts, produced only a very small decrease in the firing rate of VTA neurons but potentiated ethanol excitation of these neurons. Higher concentrations of cocaine (1 mu M) did not enhance ethanol excitation. Ethanol-induced excitation was potentiated by the higher concentrations of cocaine (1 and 2 mu M) in the presence of the D-2 receptor antagonist sulpiride (1 mu M). Furthermore, cocaine potentiation of ethanol-induced excitation was reversed by ketanserin (2 mu M), a 5-HT2 antagonist. The enhanced ethanol excitation of VTA dopaminergic neurons caused by cocaine may partially explain the high incidence of the coabuse of these two substances.

关键词：中枢神经系统抑制药/药理学可卡因/药理学多巴胺/生理学多巴胺拮抗剂/药理学多巴胺摄取抑制剂/药理学药物协同作用乙醇/药理学细胞外间隙/代谢酮色林/药理学神经元/代谢大鼠近交F344 奖励血清素拮抗药/药理学舒必利/药理学腹侧被盖区/代谢动物大鼠

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Chronic exposure to ethanol alters GABA_A receptor-mediated responses of layer II pyramidal cells in adult rat piriform cortex

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JOURNAL OF NEUROPHYSIOLOGY 2000年第1期84卷 247-254页

作者： Signore, AP Yeh, HH Univ Connecticut Ctr Hlth Program Neurosci Farmington CT 06030 USA Univ Connecticut Ctr Hlth Dept Pharmacol Farmington CT 06030 USA

This study examined the effect of chronic exposure to ethanol on gamma-aminobutyric acid type-A (GABA(A)) receptor-mediated responses of layer II pyramidal neurons of the piriform cortex. Slices containing the piriform cortex were derived from pair-fed adult rats maintained on ethanol-supplemented or control liquid diet for 30 days. Responses of identified layer II pyramidal neurons to exogenously applied GABA were monitored by whole-cell patch-clamp recording. Chronic exposure to ethanol resulted in a rightward shift in the EC50 of GABA and a decrease in the amplitude of maximal GABA response. GABA-induced responses were modulated by acutely applied ethanol (10-100 mM) in both chronic ethanol-treated and control groups. No significant difference was found in the average change in GABA response, suggesting that tolerance to acute ethanol exposure did not develop. When the modulatory responses of individual cells were classified and grouped as either being attenuating, potentiating, or having no effect, the incidence of potentiation in the ethanol-treated group was significantly higher. Consistent with the absence of tolerance to acute ethanol, cross-tolerance to diazepam was not observed following 30 days of treatment with ethanol. These results are discussed in light of regionally specific effects of chronic ethanol treatment on GABA(A) receptor-mediated responses of layer II piriform cortical neurons.

关键词：年龄因素慢性酒精中毒/病理生理学荷包牡丹碱/药理学中枢神经系统抑制药/药理学大脑皮质/细胞学大脑皮质/药物作用大脑皮质/生理学地西泮/药理学药物耐受性/生理学乙醇/药理学 GABA拮抗剂/药理学 GABA调节剂/药理学锥体细胞/化学锥体细胞/药物作用锥体细胞/生理学大鼠 Sprague-Dawley 受体 GABA-A/生理学 γ氨基丁酸/生理学动物男(雄)性大鼠

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Selectively bred lines of mice show response and drug specificity for genetic regulation of acute functional tolerance to ethanol and pentobarbital

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第1期293卷 188-195页

作者： Erwin, VG Gehle, VM Deitrich, RA Univ Colorado Hlth Sci Ctr Sch Pharm Alcohol Res CtrDept Pharmaceut Sci Denver CO 80262 USA Univ Colorado Hlth Sci Ctr Dept Pharmacol Alcohol Res Ctr Denver CO 80262 USA

Genetic regulation of acute tolerance to ethanol may be associated with ethanol consumption and other ethanol-related behaviors in rodents. We have used lines of mice, selectively bred for high and low acute functional tolerance (HAFT and LAFT, respectively) to ethanol-induced loss of balance to test this hypothesis. Replicate HAFT and LAFT lines differ in AFT to ethanol-induced loss of balance by 4.4- and 5-fold, respectively. Frequency distributions and mean AFT scores for those lines, F-1, and backcrosses show a dominance for the HAFT phenotype. Time courses for acquisition and decay showed that AFT to ethanol-induced loss of balance developed rapidly, could be maintained up to 6 h with repeated doses, and decayed 6 h after peak tolerance and discontinuance of ethanol administration. The lines did not differ in initial sensitivity as measured by brain ethanol concentration at loss of balance, indicating that initial sensitivity and AFT to loss of balance were not coselected traits. Surprisingly, HAFT versus LAFT lines did not differ in development of AFT to loss of righting response, or hypothermia, indicating different mechanisms or neuronal systems mediate genetic influences on these measures. Voluntary ethanol consumption was low in both of the replicate lines, but HAFT lines consumed greater amounts of ethanol than LAFT lines. The HAFT and LAFT lines developed AFT to pentobarbital-induced loss of balance, however, there were no line differences in rates or extent of the AFT development. These results show that genetic regulation of AFT development is drug- as well as response-specific.

关键词：饮酒/遗传学饮酒/心理学体温/药物作用体温/遗传学中枢神经系统抑制药/药理学交叉遗传剂量效应关系药物药物耐受性/遗传学乙醇/药理学催眠药和镇静药/药理学小鼠近交系运动活动/药物作用运动活动/遗传学肌肉骨骼平衡/药物作用戊巴比妥/药理学种特异性时间因素动物小鼠

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Acute effects of ethanol on kainate receptors with different subunit compositions

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第3期288卷 1199-1206页

作者： Valenzuela, CF Cardoso, RA Univ New Mexico Hlth Sci Ctr Dept Neurosci Albuquerque NM 87131 USA Univ Colorado Hlth Sci Ctr Dept Pharmacol Denver CO 80262 USA

Previous studies showed that recombinant homomeric GluR6 receptors are acutely inhibited by ethanol. This study examined the acute actions of ethanol on recombinant homomeric and heteromeric kainate (KA) receptors with different subunit configurations. Application of 25 to 100 mM ethanol produced inhibition of a similar magnitude of both GluR5-Q and GluR6-R KA receptor-dependent currents in Xenopus oocytes. Ethanol decreased the KA E-max without affecting the EC,, and its effect was independent of the membrane holding potential for both of these receptors subtypes. Ethanol also inhibited homomeric and heteromeric receptors transiently expressed in human embryonic kidney (HEK) 293 cells. In these cells, the expression of heteromeric GluR6-R subunit-containing receptors was confirmed by testing their sensitivity to 1 mM alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid. Ethanol inhibited to a similar extent KA-gated currents mediated by receptors composed of either GluR6 or GluR6 + KA1 subunits, and to a slightly lesser extent receptors composed of GluR6 + KA2 subunits. Acute ethanol's effects were tested on GluR5 KA receptors that are expressed as homomers (GluR5-Q) or heteromers (GluR5-R + KA1 and GluR5-R + KA2). Homomeric and heteromeric GluR5 KA receptors were all inhibited to a similar extent by ethanol;however, there was slightly more inhibition of GluR5-R + KA2 receptors. Thus, recombinant KA receptors with different subunit compositions are all acutely inhibited to a similar extent by ethanol. In light of recent reports that KA receptors regulate neurotransmitter release and mediate synaptic currents, we postulate that these receptors may play a role in acute ethanol intoxication.

关键词：细胞系/代谢中枢神经系统抑制药/药理学乙醇/药理学基因表达卵母细胞/代谢膜片钳术受体红藻氨酸/生物合成受体红藻氨酸/药物作用受体红藻氨酸/遗传学重组蛋白质类/药物作用转染爪蟾属动物人类

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Cocaine and alcohol interactions in the rat: Effect of cocaine and alcohol pretreatments on cocaine pharmacokinetics and pharmacodynamics

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JOURNAL OF PHARMACEUTICAL SCIENCES 1999年第12期88卷 1266-1274页

作者： Pan, WJ Hedaya, MA Washington State Univ Coll Pharm Dept Pharmaceut Sci Pharmacol Toxicol Grad Program Pullman WA 99164 USA

This experiment was designed to investigate the effect of pretreatment with cocaine and alcohol on cocaine pharmacokinetics and pharmacodynamics. Four groups of rats (n = 8 per group) received one of the following pretreatments for two weeks: none, alcohol (10% v/v in drinking water), cocaine (15 mg/kg/day ip), and alcohol+cocaine (10% v/v in drinking water+15 mg/kg/day ip). On the day of the experiment, cocaine was administered (30 mg/kg, ip) to each rat, either alone or in combination with alcohol (5 g/kg, po), in a balanced crossover experimental design. Plasma and brain ECF concentrations of cocaine and its three metabolites: benzoylecgonine, norcocaine, and cocaethylene were assayed by HPLC-UV. The percent change in brain dopamine concentration, mean arterial blood pressure, and heart rate were determined simultaneously. A sigmoid-E-max model was used to describe the brain cocaine concentration-neurochemical effect (dopamine) relationship, and an indirect pharmacodynamic response model was used to describe the plasma cocaine concentration-cardiovascular effect relationships. Alcohol pretreatment led to significant increase in cocaine AUC(p), alpha(t1/2), and beta(t1/2) Cocaine pretreatment significantly increased cocaine bioavailability, absorption rate constant, TBC, and the formation clearance of cocaethylene. Acute alcohol coadministration with cocaine increased cocaine AUC(p) and bioavailability, reduced the fraction of cocaine dose converted to benzoylecgonine, and increased the formation of norcocaine. These results indicate that the pharmacokinetics of cocaine, either administered alone or in combination with alcohol, is significantly altered due-to prior cocaine and/or alcohol use. Both cocaine and alcohol pretreatments increased the E-max for dopamine, with no effect on the EC50 Acute alcohol coadministration with cocaine significantly increased the E-max for dopamine and reduced the EC50. Cocaine pretreatment significantly decreased the I-max far bloo

关键词：算法曲线下面积生物转化血压/药物作用脑化学/药物作用中枢神经系统抑制药/药理学色谱法高压液相可卡因/类似物和衍生物可卡因/血液可卡因/代谢可卡因/药代动力学可卡因/药理学多巴胺/代谢多巴胺摄取抑制剂/血液多巴胺摄取抑制剂/药代动力学多巴胺摄取抑制剂/药理学药物相互作用乙醇/药理学心率/药物作用模型生物学大鼠 Wistar 动物男(雄)性大鼠

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Effect of chronic ethanol and withdrawal on the μ-opioid receptor- and 5-hydroxytryptamine_1A receptor-stimulated binding of [³⁵S]guanosine-5′-O-(3-thio)triphosphate in the fawn-hooded rat brain:: A quantitative autoradiography study

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第1期293卷 159-165页

作者： Chen, F Lawrence, AJ Monash Univ Dept Pharmacol Clayton Vic 3168 Australia

Previous studies have shown that chronic ethanol influences the density of central mu-opioid receptors and serotonin(1A) (5-hydroxytryptamine(1A)) receptors. To determine whether the functional coupling of these two receptors to G proteins in the rat brain, particularly in mesocorticolimbic regions, is affected by ethanol, receptor-mediated [S-35]guanosine-5'-O-(3-thio)-triphosphate ([S-35]GTP gamma S) binding stimulated by [D-Ala(2),N-MePhe(4),Gly-ol(5)]-enkephalin (DAMGO) or L694,247 was used. By quantitative autoradiography, receptor-mediated [S-35]GTP gamma S binding activated by the two agonists was mapped throughout brain sections at the level of the nucleus accumbens and hippocampus from groups of alcohol-preferring Fawn-Hooded (FH) rats after different ethanol consumption paradigms. Significant DAMGO (mu-opioid receptor agonist)-stimulated binding of [S-35]GTP gamma S was obtained in the striatum, nucleus accumbens, and lateral septum, whereas L694,247 (5-hydroxytryptamine(1A/1B/1D) receptor agonist)-stimulated binding of [S-35]GTP gamma S was observed in the lateral septum, amygdala, and cingulate cortex. Chronic ethanol self-administration significantly reduced DAMGO-stimulated [S-35]GTP gamma S binding in the nucleus accumbens (-19%), lateral septum (-15%), and striatum (-23%), which recovered toward control levels after ethanol withdrawal. However, chronic ethanol, as well as ethanol withdrawal, failed to produce any significant alteration in L694,247-stimulated [S-35]GTP gamma S binding in all tested brain regions. The region-specific and receptor-specific alteration of agonist-stimulated [S-35]GTP gamma S binding suggests that the change of functional coupling of mu-opioid receptors to G proteins induced by chronic ethanol drinking may have a pathophysiological role in the consequences of ethanol consumption.

关键词：饮酒/代谢放射自显影术脑化学/药物作用中枢神经系统抑制药/药理学脑啡肽丙(2)-甲基苯丙(4)-甘(5)-/药理学乙醇/药理学 GTP结合蛋白质类/代谢鸟苷5'-O-(3-硫代三磷酸)/药理学蛋白质结合/药物作用大鼠近交系受体阿片样 μ/药物作用受体血清素/药物作用受体血清素 5-HT1 物质戒断综合征/心理学动物男(雄)性大鼠

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Developmental changes in the modulation of synaptic glycine receptors by ethanol

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JOURNAL OF NEUROPHYSIOLOGY 2000年第5期84卷 2409-2416页

作者： Eggers, ED O'Brien, JA Berger, AJ Univ Washington Sch Med Dept Physiol & Biophys Seattle WA 98195 USA

During postnatal motoneuron development, the glycine receptor (GlyR) alpha subunit changes from alpha2 (fetal) to alpha1 (adult). To study the effect this change has on ethanol potentiation of GlyR currents in hypoglossal motoneurons (HMs), we placed neurons into two groups: neonate [postnatal day 1 to 3 (P1-3)], primarily expressing a2, and juvenile (P9-13), primarily expressing alpha1. We found that glycinergic spontaneous miniature inhibitory postsynaptic currents (mIPSCs) in neonate HMs are less sensitive to ethanol than in juveniles. Thirty millimolar ethanol increased the amplitude of juvenile mIPSCs but did not significantly change neonatal mIPSCs. However, 100 mM ethanol increased the amplitudes of both neonate and juvenile mIPSCs. There was a significant difference between age groups in the average ethanol-induced increase in mIPSC amplitude for 10, 30, 50, and 100 mM ethanol. In both age groups ethanol increased the frequency of glycinergic mIPSCs, but there was no difference in the amount of frequency increase between age groups. Ethanol (100 mM) also potentiated evoked IPSCs (eIPSCs) in both neonate and juvenile HMs. As we observed for mIPSCs, 30 mM ethanol increased the amplitude of juvenile eIPSCs, but had no significant effect on eIPSCs in neonate HMs. Ethanol also potentiated currents induced by exogenously applied glycine in both neonate and juvenile HMs. These results suggest that ethanol directly modulates the GlyR. To investigate possible mechanisms for this, we analyzed the time course of mIPSCs and single-channel conductance of the GlyR in the presence and absence of ethanol. We found that ethanol did not significantly change the time course of mIPSCs. We also determined that ethanol did not significantly change the single-channel conductance of synaptic GlyRs, as estimated by nonstationary noise analysis of mIPSCs. We conclude that the adult form of the native GlyR is more sensitive to ethanol than the fetal form. Further, enhancement of GlyR

关键词：年龄因素动物新生脑干/细胞学脑干/生长和发育脑干/生理学中枢神经系统抑制药/药理学导电性乙醇/药理学诱发电位/药物作用诱发电位/生理学甘氨酸/生理学膜电位/药物作用膜电位/生理学神经抑制/药物作用神经抑制/生理学大鼠 Sprague-Dawley 反应时间/药物作用反应时间/生理学受体甘氨酸/代谢突触/药物作用突触/代谢动物大鼠

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Genetic differences in alcohol sensitivity and the inheritance of alcoholism risk

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PSYCHOLOGICAL MEDICINE 1999年第5期29卷 1069-1081页

作者： Heath, AC Madden, PAF Bucholz, KK Dinwiddie, SH Slutske, WS Bierut, LJ Rohrbaugh, JW Statham, DJ Dunne, MP Whitfield, JB Martin, NG Washington Univ Sch Med Dept Psychiat St Louis MO 63110 USA Univ Missouri Dept Psychol Columbia MO USA Chicago Med Sch Dept Psychiat N Chicago IL USA Queensland Inst Med Res Dept Epidemiol & Populat Hlth Brisbane Qld 4006 Australia Queensland Univ Technol Dept Epidemiol Brisbane Qld Australia Royal Prince Alfred Hosp Dept Clin Biochem Sydney NSW Australia

Background. Substantial evidence exists for an important genetic contribution to alcohol dependence risk in women and men. It has been suggested that genetically determined differences in alcohol sensitivity may represent one pathway by which an increase in alcohol dependence risk occurs. Methods. Telephone interview follow-up data were obtained on twins from male, female and unlike-sex twin pairs who had participated in an alcohol challenge study in 1979-81, as well as other pairs from the same Australian twin panel surveyed by mail in 1980-82. Results. At follow-up, alcohol challenge men did not differ from other male twins from the same age cohort on measures of lifetime psychopathology or drinking habits;but alcohol challenge women were on average heavier drinkers than other women. A composite alcohol sensitivity measure, combining subjective intoxication and increase in body-sway after alcohol challenge in 1979-81, exhibited high heritability (60%). Parental alcoholism history was weakly associated with decreased alcohol sensitivity in women, but not after adjustment for baseline drinking history, or in men. High alcohol sensitivity in men was associated with substantially reduced alcohol dependence risk (OR = 0.05, 95% CI 0.01-0.39). Furthermore, significantly decreased (i.e;low) alcohol sensitivity was observed in non-alcoholic males whose MZ co-twin had a history of alcohol dependence, compared to other non-alcoholics. These associations remained significant in conservative analyses that controlled for respondents' alcohol consumption levels and alcohol problems in 1979-81. Conclusions. Men (but not women) at increased genetic risk of alcohol dependence (assessed by MZ co-twin's history of alcohol dependence) exhibited reduced alcohol sensitivity. Associations with parental alcoholism were inconsistent.

关键词：慢性酒精中毒/病因学慢性酒精中毒/遗传学中枢神经系统抑制药/药理学乙醇/药理学疾病遗传易感性危险性评估性别因素成年人女(雌)性人类男(雄)性中年人

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