• Title/Summary/Keyword: 알콜대사

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Mycelial Culture of Lentinus edodes Alleviates Rat Liver Toxicity Induced by Carbon Tetrachloride and Ethanol (표고버섯균사체의 사염화탄소 및 알콜로 처리된 흰쥐 간기능 보호 효과)

  • Ha, Yeong-L.;Kim, Young-S.;Ahn, Chae-R.;Kweon, Jung-M.;Park, Cherl-W.;Ha, Young-K.;Kim, Jeong-O.
    • Journal of Life Science
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    • v.20 no.1
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    • pp.133-141
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    • 2010
  • The protective effect of a mixed powder from solid-cultured and liquid-cultured Lentinus edodes mycelia (2:1, w/w) (designate LED) on the carbon tetrachloride ($CCl_4$)- and ethanol-induced hepatotoxicity of male Sprague-Dawley (SD) rat was investigated. In the $CCl_4$-induced rat hepatotoxicity experiment, rats of 4 groups (6 rats/group) were administere with Normal (0.2 ml distilled water), Control (0.2 ml distilled water), LED (LED 200 mg/kg BW + 0.2 ml distilled water), and Silymarin (200 mg/kg BW + 0.2 ml distilled water), p.o., daily for 2 weeks. Afterwards, all groups except for the Normal group were subjected to abdominal injection with $CCl_4$ ($CCl_4$ : corn oil, 1:1 v/v; 0.5 ml/kg BW). For the ethanol- induced rat hepatotoxicity experiment, rats were divided into 5 groups (5 rats/group): Normal; Pair-fed control (PFC); Control (ethanol); LED (ethanol + LED 200 mg/kg BW); and Silymarin (ethanol + silymarin 200 mg/kg BW). Rats of the Normal and PFC groups were fed a basal liquid diet, and rats of the Control, LED, and Silymarin groups were fed a liquid ethanol diet containing LED or Silymarin. Eight weeks later, blood and liver samples were collected to analyze biomarkers. In $CCl_4$-induced SD rats, LED elevated hepatic superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH peroxidase) activities and thiobarbituric reactive substances (TBARS) were reduced, resulting in the reduction of glutamate-oxalate transaminase (GOT), glutamate-pyruvate transaminase (GPT) and lactic dehydrogenase (LDH) activities in plasma. Similar results of these enzymes and biochemical markers in both liver tissues and plasma were seen in ethanol-induced hepatotoxicity of SD rats. In addition, elevated alcohol dehydrogenase (ADH) activity and reduced expression of cytochrome p450 mixed monooxygenase enzyme (CYP2E1) were seen in liver tissues from ethanol-treated rats by LED treatment. These effects of LED were similar to those of Silymarin. In in vitro experiments, LED showed antioxidant activity in a 2,2-diphenyl-1-picrylhydrazyl (DPPH) system and mouse liver mitochondria system induced by NADPH/$Fe^{2+}$ and cumine hydroperoxide (CuOOH). These results indicate that LED protected SD rat hepatotoxicity, induced by $CCl_4$ and ethanol, through its antioxidative activity and might be useful as a material for protection from hepatoxicity in humans.

Effect of Acute Ethanol Intoxication on the Pulmonary Compliance and Surfactant in Rats (급성(急性) Ethyl 알콜 중독(中毒) 흰쥐의 폐용압률(肺容壓率)과 폐포활성물질(肺胞活性物質)의 변화(變化))

  • Lee, Seung-Jung;Choo, Young-Eun
    • The Korean Journal of Physiology
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    • v.15 no.1
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    • pp.27-36
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    • 1981
  • Relatively little has been done on the metabolic changes of the lung produced by the excessive alcohol ingestion to the point of the acute alcohol intoxication. In the present study, an effort was made to clarify the possible changes of the pulmonary surfactant system by the acute alcohol ingestion. The dynamic pulmonary compliance and the levels of protein and inorganic phosphorus (Pi) of both lung lavage and extract were chosen as the parameters of the pulmonary surfactant activities. The albino rats of both sexes were used, and 1.5 ml of 50% ethanol per 100 g body weight was given by oral intubation, and the experiment was performed at 1, 3, 6, 12, and 24 hours after the alcohol ingestion. The rat was sacrificed by cutting the carotid arteries, and blood sample for the determination of hematocrit(Hct) and the blood alcohol concentration was obtained. Both lungs were completely removed without dammage to the lung tissue, and the pulmonary compliance was measured by the changes of pressure-volume(P-V) curves by inflating or deflating the lung with air. Immediately after the P-V curves were recorded, the lung lavage was obtained by washing the lobes with 15ml of isotonic saline 3 times with a syringe. Next, total lungs were homogenized and filtered to obtain the lung extract. The protein and Pi levels were measured using the lung lavage and extract as the samples, and the lung/body weight ratio(L/B ratio) was also calculated. The results thus obtained were compared with the normal values and summarized as follows. The blood alcohol concentration reached the highest level of $0.71{\pm}0.02\;g\;%$ at 1 hr and gradually decreased until 24 hrs$(0.36{\pm}0.02\;g%)$ after the alcohol ingestion, but all the experimental groups showed significant increase comparing with the normal. The highest Hct value was obtained at 1hr$(64.86{\pm}2.45%)$ and significantly elevated value was continued throughout the experiment. The L/B ratio was significantly lowered from 3hrs until 24hrs after the alcohol ingestion but from 6 th hr on, a generally elevated value was observed with a significant value at 12 hrs and gradual recovery to the normal value at 24 hrs after the alcohol ingestion. The pulmonary compliance at inflation and deflation did not change appreciablly from the normal until 3 hrs after the alcohol ingestion but from 6 th hr on, a generally elevated value was observed with a significant value at 12 hrs and gradual recovery to the normal value at 24 hrs after the alcohol ingestion. The protein level of the lung lavage stowed a significantly increased value of $12.36{\pm}0.35\;mg/gm(3rd hr)$, $12.70{\pm}0.74\;mg/gm(12 th hr)$, and $12.65{\pm}0.88\;mg/gm(24 th hr)$, respectively, comparing with the normal value of $10.65{\pm}0.62\;mg/gm$, and the Pi level also showed a similar tendency of significant increase at 12th hr $(7.65{\pm}0.63\;{\mu}mol/gm)$ and 24 th hr$(6.70{\pm}0.36\;{\mu}mol/gm)$ comparing with the normal value of $5.32{\pm}0.20\;{\mu}mol/gm$. The protein level of the lung extract in the alcohol group was generally similar to the normal value with a slight decrease at 1st and 3 rd hr, tut the Pi level of the lung extract was generally increased in the alcohol group, and a significant increase was observed at 6 th hr$(17.77{\pm}1.54\;{\mu}mol/gm)$, 12 th hr$(13.92{\pm}0.78\;{\mu}mol/gm)$ and 24 th hr$(14.57{\pm}0.53\;{\mu}mol/gm)$ of the alcohol ingestion comparing with the normal value of $10.34{\pm}0.37\;{\mu}mol/gm$. From the above, it may be concluded that the acute alcohol intoxication produces the metabolic changes of the lungs by the increased surfactant activities and elevated pulmonary compliance.

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