顶空气相色谱法快速测定血中甲醇与乙醇的含量

目的 :建立一种简便、快速测定血浆中甲醇、乙醇浓度的顶空气相色谱法 ,并与直接进样法测定结果进行比较。方法 :外标法定量 ,分析柱为GDX -102玻璃填充柱 ,载气为N2,检测器为FID ;0.5ml血浆样品以小瓶密封 ,25℃下平衡20min ,用气密性注射器取顶空进样1.0ml。结果 :本法甲醇和乙醇的线性范围为0.2～7.5g/L ;日内RSD<4 % ,日间RSD<5.5 % ;方法回收率甲醇为(100.9±3.8) % ,乙醇为 (101.5±3.4) % ;最低检测限<0.01g/L。结论 :本法操作简便、快速 ,灵敏度高 ,结果准确可靠     

Effect of Ethanol on Uterotropic Action of Estrogens

Female rats aging 3 months at the beginning of experiments received 5 or 15% ethanol and then were subjected to bilateral ovariectomy 2 weeks before end of the experiment. During the last 11 days they were daily injected intramuscularly with 2 g estradiol. Drinking of 5% ethanol combined with injections of estrogens induced DNA damage in the uterus detected by comet assay and abolished induction of progesterone receptors, changes in peroxidase activity, proliferation index, endometrium thickness, and other indices reflecting the hormonal effect of estradiol on the uterus. Drinking of 15% ethanol was accompanied by an increase in DNA-damaging effects of estrogens and a decrease in their hormonal uterotropic effects. It is concluded that unlike tobacco smoking, drinking of moderate ethanol concentrations modifies primarily genotoxic, but not the hormonal effect of estrogens.     

Chronic ethanol intake modifies pyrrolidon carboxypeptidase activity in mouse frontal cortex synaptosomes under resting and K+ -stimulated conditions: role of calcium

Pyrrolidon carboxypeptidase (Pcp) is an omega peptidase that removes pyroglutamyl N-terminal residues of peptides such as thyrotrophin-releasing hormone (TRH), which is one of the neuropeptides that has been localized into many areas of the brain and acts as an endogenous neuromodulator of several parameters related to ethanol (EtOH) consumption. In this study, we analysed the effects of chronic EtOH intake on Pcp activity on mouse frontal cortex synaptosomes and their corresponding supernatant under basal and K+ -stimulated conditions, in presence and absence of calcium (Ca2+) to know the regulation of Pcp on TRH. In basal conditions, chronic EtOH intake significantly decreased synaptosomes Pcp activity but only in absence of Ca2+. However, supernatant Pcp activity is also decreased in presence and absence of calcium. Under K+-stimulated conditions, chronic EtOH intake decreased synaptosomes Pcp activity but only in absence of Ca2+, whereas supernatant Pcp activity was significantly decreased only in presence of Ca2+. The general inhibitory effect of chronic EtOH intake on Pcp activity suggests an inhibition of TRH metabolism and an enhancement of TRH neurotransmitter/neuromodulator functions, which could be related to putative processes of tolerance to EtOH in which TRH has been involved. Our data may also indicate that active peptides and their degrading peptidases are released together to the synaptic cleft to regulate the neurotransmitter/neuromodulator functions of these peptides, through a Ca2+ -dependent mechanism.     

Effect of ethanol-wet bonding with hydrophobic adhesive on caries-affected dentine

Frequently encountered in clinical practice, caries-affected dentine (CAD) is the most challenging bonding substrate. This study evaluated the effect of ethanol-wet bonding with hydrophobic adhesive to sound dentine and to CAD. In the control groups, prepared sound dentine and CAD were bonded with Adper Single Bond 2 using a traditional water-wet bonding technique. In the experimental groups, the specimens were treated as follows: Group 1, rinsed with stepwise ethanol dehydration; Group 2, immersion in 100% ethanol, three times, for 20 s each time; and Group 3, immersion in 100% ethanol for 20 s. Microtensile bond strength (μTBS) testing was used to evaluate the effects of the different protocols on bonding. The microhardness of debonded dentine surfaces was measured to ensure the presence of CAD. Interfacial nanoleakage was evaluated by field-emission scanning electron microscopy. Treatment significantly improved the μTBS in CAD in Groups 1 and 2, but had no effect on Group 3. Conversely, treatment significantly reduced the μTBS in sound dentine in Groups 2 and 3, but had no effect in Group 1. The presence of nanoleakage varied with the ethanol-wet protocol used. In conclusion, ethanol-wet bonding can potentially improve bond efficacy to CAD when an appropriate protocol is used.     

Water/Ethanol Selectivity of New Organic‐Inorganic Hybrid Membranes Fabricated from Poly(vinyl alcohol) and an Oligosilane

To control the swelling of PVA membranes, mixtures of PVA and an inorganic oligosilane were prepared using sol‐gel reactions to yield new PVA/oligosilane hybrid membranes. In the separation of an ethanol/water azeotropic mixture during pervaporation, the effect of the oligosilane content on the water/ethanol selectivity of PVA/oligosilane hybrid membranes was investigated. The water/ethanol selectivity of PVA/oligosilane hybrid membranes was higher than that of PVA membranes, but the water/ethanol selectivity of hybrid membranes decreased with increasing oligosilane content. In order to increase the water/ethanol selectivity, PVA/oligosilane hybrid membranes were annealed. The water/ethanol selectivity of annealed PVA/oligosilane hybrid membranes was greater than un‐annealed hybrid membranes, and significantly governed by the oligosilane content, which could be attributed to both sorption and diffusion selectivities. The relationship between the structure of un‐annealed and annealed PVA/oligosilane hybrid membranes along with permeation and separation characteristics of an ethanol/water azeotropic mixture during pervaporation are discussed in detail.

     

Alcohol, athletic performance and recovery

Alcohol consumption within elite sport has been continually reported both anecdotally within the media and quantitatively in the literature. The detrimental effects of alcohol on human physiology have been well documented, adversely influencing neural function, metabolism, cardiovascular physiology, thermoregulation and skeletal muscle myopathy. Remarkably, the downstream effects of alcohol consumption on exercise performance and recovery, has received less attention and as such is not well understood. The focus of this review is to identify the acute effects of alcohol on exercise performance and give a brief insight into explanatory factors.     

Ethanol promotes neuronal apoptosis by inhibiting phosphatidylserine accumulation

Prenatal and postnatal ethanol exposure induces abnormal cell death in the nervous system. We have previously reported that docosahexaenoic acid (DHA; 22:6n-3) prevents neuronal apoptosis through promoting phosphatidylserine (PS) accumulation. Previously, we have shown in C6 glioma cells that ethanol inhibits the accumulation of PS caused by DHA supplementation. In this report, we demonstrate that in vitro or in vivo exposure to ethanol inhibits DHA-dependent PS accumulation and neuronal survival. We found that Neuro 2A cells exposed to ethanol accumulated considerably less PS in response to the DHA enrichment and were less effective at phosphorylating Akt and suppressing caspase-3 activity under serum-starved or staurosporine-treated conditions. The in vivo paradigm correlated well with the in vitro findings. We found that the total PS and DHA contents in the fetal hippocampus were slightly but significantly lowered by the prenatal ethanol exposure. Fetal hippocampal cultures obtained at embryonic day 18 from ethanol-treated pregnant rats contained significantly higher apoptotic cells after 7 days in vitro under basal conditions and exhibited particular susceptibility to cell death induced by trophic factor removal in comparison with the pair-fed control group. The reduction of PS and the resulting neuronal cell death inappropriately enhanced during development may contribute to the defects in brain function often observed in fetal alcohol syndrome.     

Alcohol increases efficacy of immature synapses in a neurosteroid-dependent manner

Fetal ethanol exposure persistently affects hippocampal circuits leading to learning and memory disabilities. Although the mechanisms responsible for these effects are not fully understood, several studies implicate neurosteroids as mediators of the actions of ethanol. A neurosteroid that appears to be critical for the fetal actions of ethanol is pregnenolone sulfate (PREGS). We found that chronic prenatal ethanol exposure increases PREGS levels in the fetal brain and that an endogenous PREGS-like neurosteroid strengthens excitatory transmission in the neonatal hippocampus. Therefore, we hypothesized that ethanol could affect synaptic transmission in the developing hippocampus in a PREGS-dependent manner. We used patch-clamp electrophysiological techniques and found that 50 mm ethanol strengthens AMPA receptor-mediated transmission in the CA1 region by reducing the failure rate of low-efficacy synapses. This effect was age-dependent and was occluded by application of exogenous PREGS. An anti-PREGS antibody scavenger and blockade of PREGS synthesis prevented the effect of ethanol. These data indicate that the deleterious effects of ethanol on hippocampal development are mediated in part by alterations in neurosteroid production, which results in premature stabilization of excitatory synapses.     

Taurine elevates dopamine levels in the rat nucleus accumbens; antagonism by strychnine

The mesolimbic dopamine (DA) system, projecting from the ventral tegmental area (VTA) to the nucleus accumbens (nAcc), is involved in reward-related behaviours and addictive processes, such as alcoholism and drug addiction. It was recently suggested that strychnine-sensitive glycine receptors (GlyR) in the nAcc regulate both basal and ethanol-induced mesolimbic DA activity via a neuronal loop involving endogenous activation of nicotinic acetylcholine receptors (nAChR) in the VTA. However, as the nAcc appears to contain few glycine-immunoreactive cell bodies or fibres, the question as to what may be the endogenous ligand for GlyRs in this brain region remains open. Here we have investigated whether the amino acid taurine could serve this purpose using in vivo microdialysis in awake, freely moving male Wistar rats. Local perfusion of taurine (1, 10 or 100 mm in the perfusate) increased DA levels in the nAcc. The taurine (10 mm)-induced DA increase was, similarly to that previously observed after ethanol, completely blocked by (i) perfusion of the competitive GlyR antagonist strychnine in the nAcc, (ii) perfusion of the nAChR antagonist mecamylamine (100 microm) in the VTA, and (iii) systemic administration of the acetylcholine-depleting drug vesamicol (0.4 mg/kg, i.p). The present results suggest that taurine may be an endogenous ligand for GlyRs in the nAcc and that the taurine-induced elevation of DA levels in this area, similarly to that observed after local ethanol, is mediated via a neuronal loop involving endogenous activation of nAChRs in the VTA.