Ethanol pretreatment with

Concerning ulcers induced by absolute ethanol, pretreatment with silymarin stimulated mucus secretion, but did not modify the concentration of total proteins and hexosamines [99]. By contrast, in the same experimental model, Reyes et al. [98] found that mucus amount was not modified by the ethylacetate extract of Erica andevalensis, although there was an increase in the concentration of its components. Perez-Guerrero et al. [113] showed that rutin, the glycoside of quercetin, has a protective effect, although it did not induce any changes in the amount of mucus or in its glycoprotein content. 

The hepatic microsomal a-hydroxylase activity for NPYR is inducible in rats by pretreatment with Aroclor, and in hamsters by pretreatment with Aroclor, 3-methylcholanthrene, phenobarbi-tal, and ethanol (10,15,19). In contrast, pretreatment of rats with 3-methylcholanthrene or phenobarbital causes no change or a slight decrease in microsomal NPYR o-hydroxylase activity (19). 

Male Wistar rats were administered 330 or 660 mg/kg of ethanol intraperitoneally 30 minutes before being exposed to 800 ppm of hydrogen sulfide for a maximum of 20 minutes, which was a potentially fatal hydrogen sulfide exposure (Beck et al. 1979). Mean times to unconsciousness in animals that were exposed to hydrogen sulfide with ethanol pretreatment at either of these dose levels were approximately 35% less than times to unconsciousness without ethanol pretreatment (Beck et al. 1979). The clinical relevance of these findings, which used potentially fatal doses of both ethanol and hydrogen sulfide, is unclear. 

Shier, W.T., Koda, L.Y., and Bloom, F.E., Metabolism of pi I dopamine following intracerebroven-tricular injection in rats pretreated with ethanol or choral hydrate, Neuropharmacology, 22, 279, 1983. 

The application of flavonoids for the treatment of various diseases associated with free radical overproduction is considered in Chapter 29. However, it seems useful to discuss here some studies describing the activity of flavonoids under certain pathophysiological conditions. Oral pretreatment with rutin of rats, in which gastric lesions were induced by the administration of 100% ethanol, resulted in the reduction of the area of gastric lesions [157]. Rutin was found to be an effective inhibitor of TBAR products in the gastric mucosa induced by 50%i ethanol [158]. Rutin and quercetin were active in the reduction of azoxymethanol-induced colonic neoplasma and focal area of dysplasia in the mice [159], Chemopreventive effects of quercetin and rutin were also shown in normal and azoxymethane-treated mouse colon [160]. Flavonoids exhibited radioprotective effect on 7-ray irradiated mice [161], which was correlated with their antioxidative activity. Dietary flavones and flavonols protected against the toxicity of the environmental contaminant dioxin [162], Rutin inhibited ovariectomy-induced osteopenia in rats [163],... 

A new HP-TLC method has been applied for the quantitative analysis of flavonoids in Passiflora coerulea L. The objective of the experiments was the separation and identification of the compound(s) responsible for the anxiolytic effect of the plant. Samples were extracted with 60 per cent ethanol or refluxed three times with aqueous methanol, and the supernatants were employed for HPTLC analysis. Separation was performed on a silica layer prewashed with methanol and pretreated with 0.1 M K2HP04, the optimal mobile phase composition being ethyl acetate-formic acid-water (9 1 l,v/v). It was established that the best extraction efficacy can be achieved with 60 - 80 per cent aqueous methanol. The HPTLC technique separates 10 different flavonoids, which can be used for the authenticity test of this medicinal plant [121],... 

X 10"3 M G-6-P, 1.6 units G-6-P dH, 5.1 X 10 5 M NADP, 1.0 mg aldrin in 0.2 ml ethanol when used alone, or 1.0 mg aldrin and 1.0 mg PBO, each in 0.1 ml ethanol, when used in combination. In synergism experiments, mixtures were pretreated with PBO for 3-5 min prior to the addition of substrate. The reaction mixtures were incubated with agitation in test tubes at 30 - 1°C in a water bath shaker for 15 min. Reactions were stopped by acidifying with 2 ml 5% TCA. The acidified mixtures were extracted and analyzed by GLC. 

Several animal studies indicate that chloroform interacts with other chemicals within the organism. The lethal and hepatotoxic effects of chloroform were increased by dicophane (DDT) (McLean 1970) and phenobarbital (a long-acting barbiturate) in rats (Ekstrom et al. 1988 McLean 1970 Scholler 1970). Increased hepatotoxic and nephrotoxic effects were observed after interaction with ketonic solvents and ketonic chemicals in rats (Hewitt and Brown 1984 Hewitt et al. 1990) and in mice (Cianflone et al. 1980 Hewitt et al. 1979). The hepatotoxicity of chloroform was also enhanced by co-exposure to carbon tetrachloride in rats (Harris et al. 1982) and by co-exposure to ethanol in mice (Kutob and Plaa 1962). Furthermore, ethanol pretreatment in rats enhanced chloroform-induced hepatotoxicity (Wang et al. 1994) and increased the in vitro metabolism of chloroform (Sato et al. 1981). 

Haloalkanes. Certain haloalkanes and haloalkane-containing mixtures have been demonstrated to potentiate carbon tetrachloride hepatotoxicity. Pretreatment of rats with trichloroethylene (TCE) enhanced carbon tetrachloride-induced hepatotoxicity, and a mixture of nontoxic doses of TCE and carbon tetrachloride elicited moderate to severe liver injury (Pessayre et al. 1982). The researchers believed that the interaction was mediated by TCE itself rather than its metabolites. TCE can also potentiate hepatic damage produced by low (10 ppm) concentrations of carbon tetrachloride in ethanol pretreated rats (Ikatsu and Nakajima 1992). Acetone was a more potent potentiator of carbon tetrachloride hepatotoxicity than was TCE, and acetone pretreatment also enhanced the hepatotoxic response of rats to a TCE-carbon tetrachloride mixture (Charbonneau et al. 1986). The potentiating action of acetone may involve not only increased metabolic activation of TCE and/or carbon tetrachloride, but also possible alteration of the integrity of organelle membranes. Carbon tetrachloride-induced liver necrosis and lipid peroxidation in the rat has been reported to be potentiated by 1,2- dichloroethane in an interaction that does not involve depletion of reduced liver glutathione, and that is prevented by vitamin E (Aragno et al. 1992). 

It exerts its action by inhibiting aldehyde dehydrogenase enz5une. Disulfiram thus increases the concentration of acetaldehyde in body when ethanol is ingested by an individual pretreated with disulfiram. The symptoms and signs produced... 

Elovaara, E., Engstrom, K., Hayri, L., Hase, T. Aitio, A. (1989) Metabolism of antipyrine and OT-xylene in rats after prolonged pretreatment with xylene alone or xylene with ethanol, phenobarbital or 3-methylcholanthrene. Xenobiotica, 19, 945-960... 

Figure 5. Scanning electron micrographs of rat gastric mucosa 1 h after administration of ethanol On the left, loss of the interpit cells with complete surface desquamation and exposure of the lamina propria on the right, pretreatment with (R)a-methylhistamine 100 mg/kg intragastrically caused the migration of pit cells with restitution of the mucosal surface (magnification x 640).

Erythrocytes from ethanol-injected fish permeated more water than those from normal fish. Water permeation was significantly enhanced with Merc cor 30 and Nux vom 30 as compared to the control. RBCs from fish pretreated with Nux vom 30 inbibed more water in in vitro treatments than those from fish pre-treated with Ethanol 30. Since aquaporins are mainly responsible for water transport through the plasma membrane of red blood cells it is thought that potentized drugs such as Merc cor 30 and Nux vom 30 acted upon these proteins and facilitated water influx into the cells (Sukul et al., 2003). 

Table 5 shows the achieved ethanol concentrations after 24 h of fermentation and the calculated ethanol yield as percent of theoretical. After 1 d of fermentation the ethanol concentrations varied from 12.1 to 13.8 g/L, corresponding to 78.4 and 90.3% of the theoretical yield. Glucose was totally consumed after 6 h of fermentation following pretreatment with 0.5% H2S04. The maximum ethanol concentration was also reached after 6 h in these cases, but when 2% H2S04 was used in pretreatment, glucose was consumed more slowly and the formation of ethanol needed more time. However, even in these cases the achieved ethanol yield was about 85% of the theoretical. These results are quite similar to those achieved after fermentation of wet oxidized wheat straw in a previous study (17). 

Many favor dilute sulfuric acid pretreatment because both high hemicellulose recovery and good cellulose digestibility can be achieved (6-8). Moreover, most of the soluble sugars from dilute-acid pretreatment are released as monomers that can be readily fermented to ethanol by recombinant organisms (9,10). Pretreatment with just hot water or steam, termed uncatalyzed hydrolysis or autohydrolysis, eliminates chemical additives, lowers the cost of materials of construction, and generates less waste, but hemicellulose and cellulose yields from batch systems are limited. 

In contrast, the energy gain of ethanol fermentation from a cellulose-based crop was estimated at only 10% [31]. A fife cycle assessment of bioethanol from wood came to a similar conclusion [32]. This unsatisfactory outcome mainly results from the energy-intensive pretreatment with steam explosion, such as is used by Iogen [16]. The replacement of the latter by COz explosion [33] may redress the energetic balance. 

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