• 동아시아식생활학회지
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• 제7권1호
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• pp.21-27
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• 1997

To evaluate the effect of ethanol pretreatment on the liver and serum xanthine oxidase(XO) activity, the bromobenzene(40mg/kg body wt., i.p.) was orally given 3 times daily to the Sprague-Dawley male rats pretreated with 5% ethanol throughout 2 months. Bromobenzene treated rats pretreated with ethanol showed the more decreased activity of serum and liver XO, and lower value of V than those of only bromobenzene treated rats. Bu the bromobenzene treatment, ethanol pretreated rats showed the more decreased levels of serum alanine aminotransferase activity and liver weight/bo여 weight(%), and decreased degree of liver damage on histopathological observation than the control group.

• Toxicological Research
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• 제20권1호
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• pp.63-69
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• 2004

Casapse-3 protease is known as a key role of apoptotic enzyme, and caspase-3 activity is a central event that occurs upstream of DNA fragmentation during apoptosis. This study demonstrates that chitosan pretreatment inhibits cadmium-induced apoptosis by attenuating the activity of caspase-3. We also analyzed the protective effect of chitosan on DNA fragmentation induced by cadmium. Cadmium toxicity was examined by DNA fragmentation and nuclear condensation with Hoechst stain. Caspase-3 activities were increased cadmium treated group for 3 hours compared with control. When chitosan (150 mg/ml) was pretreated at 30 min before cadmium treatment, cadmium cytotoxicity was suppressed in a dose-dependent manner evaluated by DNA fragmentation and caspase activity. From these results, it is suggest that the protective effect of chitosan pretreatment against cadmium-induced cytotoxicity is mediated through inhibition of caspase-3 protease activation and DNA fragmentation.

• 대한수의학회지
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• 제15권2호
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• pp.199-201
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• 1975

In order to investigate the effect of aconitine upon the parasympathetic innervation, the isolated rabbit duodenal preparation pretreated with atropine and tetrodotoxin were observed. The results obtained in this work were summerized as follows: 1. The excitatory response was evoked by the administration of aconitine ($100{\mu}g/ml$). 2. The contraction was blocked by the pretreatment with atropine ($10{\mu}g/ml$). 3. The contraction was completely blocked by the pretreatment with tetrodotoxin($10{\mu}g/ml$). These experimental evidences indicate that the excitatory response by aconitine is due to the parasympathetic nerves.

• Environmental Analysis Health and Toxicology
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• 제16권1호
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• pp.17-20
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• 2001

The alkaline comet assay, employing a single-cell gel electrophoresis(SCGE), is a rapid, simple and sensitive technique for visualizing and measuring DNA damage leading to strand breakage in individual mammalian cells. The protecting effect of pretreatment with vitamin C and cysteine on the DNA damage of gamma ray was investigated in mice splenic lymphocytes. Vitamin C and cysteine were administered orally for five consecutive days before irradiation. Four week old ICR male mice were irradiated wish 3.5Gy of γ-radiation and were sacrificed 3 days later. Spleens were taken for DNA damage examination by Comet assay and the tail moments of DNA single -strand breaks in tole splenic lymphocytes were evaluated. The results show that pretreatment with vitamin C and cysteine were effective in protecting against DNA damage by gamma ray. Administration of antioxidants like vitamin C and cysteine to mice before irradiation was effective in reducing the tail moment of splenic lymphocytes DNA.

• Advances in Traditional Medicine
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• 제4권2호
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• pp.95-99
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• 2004

The ethanolic extract of some medicinal plants having anti-asthmatic activity such as Solanum xanthocarpum, Curcuma longa, Glycyrrhiza glabra, Piper longum, A. vasica, A. lebbeck, and Tinospora cordifolia was evaluated for antihistaminic and anti-cataleptic activity. The aqueous solution of ethanolic extract of S. xanthocarpum and G. glabra potentiated histamine-induced tracheal chain contractions. Whereas, C. longa, P. longum, and T. cordifolia, and A. lebbeck were without any significant effect on histamine. Only A. vasica inhibited histamine-induced tracheal chain contraction. G. glabra per se produced contraction of the tracheal chain, which was blocked by pretreatment with atropine. Single dose of S. xanthocarpum potentiated clonidine-induced catalepsy but on repeated doses (once in a day for 3 days) inhibited catalepsy. Pretreatment with ethanolic extract of C. longa, P. longum, T. cordifolia inhibited catalepsy whereas G. glabra and A. lebbeck significantly potentiated clonidine-induced catalepsy. None of the extracts inhibited haloperidol-induced catalepsy. Thus the extracts having antihistaminic activity or mast cell stabilizing activity inhibited clonidineinduced catalepsy.

• 한국식품영양과학회지
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• 제23권2호
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• pp.181-186
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• 1994

The present study was undertaken to clarify the effect of Puffer fish skin extract (PF) on the hepatic alcohol metabolism in rats. It was observed that alcohol concentration in blood had been markedly decreased by the pretreatment of PF for two weeks. Activities of alcohol dehydrogenase (ADH) and microsomal ethanol-oxidizing system (MEOS) were significantly incrased (more than 20% of control) by pretreatment of PF for two weeks and acute alcohol intoxication (5 g/kg) on final day. When rats were fed with subacute toxic state by alcohol (25v/v % , once a day for six weeks), activities of ADH and MEOS were significantly increased by additional treatments of PF for final two weeks. But the catalase activity was not affected by any of both case. And also activities of ADH and MEOS in vitro were not changed . These results suggest that PF treatemnt prompted the recovery from alcohol intoxication.

• 한국식품영양과학회지
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• 제23권2호
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• pp.187-191
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• 1994

The present stduy was undertaken to investigate the possible effect of Puffer fish skin extract (Pf) on the heptic acetaldehyde metabolism . It was obsrved that PF markedly decreased the acetaldehyde levels in blood and liver. The activity of mitochondrial aldehyde dehydrogenase (Ald DH) increased by induction of acute intoxicatiion of alcohol (5 g/kg) was further increased through pretreatment with PF for 2 weeks. When PF was given to rat fed with 25% alcohol solution instead of water for 6 weeks. the activity of Ald DH in mitochondrial fraction decreased to about 28% compared with sucrose-treated group. But after pretreatemnt of PF, the activity was restored to the normal level. By the treatment with disulfiram (300 mg/kg, once a day for 3days) was restored to the control after the pretreatment with PF. And also mitochondrial Ald DH activity in vitro was not changed. All these observations suggest that reduction of acetaldehyde levels are partly due to increase activity of mitochondrial Ald DH. Therefore, the recovery from intoxication of acetaldehyde may be enhanced by treatment with PF.

• 환경생물
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• 제31권4호
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• pp.376-382
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• 2013

[6]-Gingerol, a major polyphenol of ginger (Zingiber officinale), exhibits a variety of biological properties including anti-oxidant, anti-inflammatory and anti-cancer activity. However, the radioprotective effect of [6]-gingerol is still unknown. The aim of this study was to investigate the radioprotective effect of [6]-gingerol against radiation-induced cell cytotoxicity and oxidative stress in HepG2 cells. [6]-Gingerol pretreatment attenuated radiation-induced cell cytotoxicity caused by 5Gy (half lethal dose, $LD_{50}$ of HepG2 cells). The measurements of superoxide dismutase (SOD) and catalase (CAT) activity were also performed. The results showed that [6]-gingerol pretreatment reduced increasing SOD and CAT activity after exposure of IR, indicating that [6]-gingerol protected oxidative stress by regulating cellular antioxidant enzyme (SOD and CAT) activity. These findings suggest that [6]-gingerol acts as a radioprotector by attenuating cell cytotoxicity and oxidative stress.

• 상하수도학회지
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• 제19권3호
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• pp.312-317
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• 2005

The 15 month pilot study was performed to investigate the effect of pretreatment by monochloramine ($NH_2Cl$) on the performance of RO membranes made of cellulose acetate (CA) and polyamide (PA). Both RO membranes experienced severe biological fouling without any pretreatment during the treatment of highly organic surface water in Florida, USA. Feed monochloramination at 5 mg/L significantly minimized productivity loss by effective control of biofouling. The CA membrane did not show any structural damages by monochloramine, while the PA membrane suffered from a gradual loss of membrane integrity by chlorine oxidation, which was characterized as an increase in productivity and a decrease in selectivity. The degradation of PA membrane increased with increasing monochloramine dose.

• Toxicological Research
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• 제6권1호
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• pp.51-59
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• 1990

Effects of altering hepatic mixed-function oxidase (MFO) enzyme activities on the metabolism and acute toxicity of parathio were investigated in adult female rats. In vitro hepatic metabolism of parathion to paraoxon was increased by phenobarbital pretreatment (50 mg/kg/day, ip, for 4 consecutive days) and SKF 525-A (50 mg/kg, ip, 1 hr prior to sacrifice) decreased paraoxon formation indicating that phenobarbital induces that form(s) of cytochrome P-450 catalyzing conversion of parathion to paraoxon. Degradation of paraoxon to p-nitrophenol was increased by phenobarbital pretreatment, but not affected by SKF 525-A suggesting that MFO activities play only a minor role in the detoxification of the active metabolite of this insecticide. The phenobarbital-induced increase in paraoxon formation was partially antagonized by SKF 525-A. Significant activity for both parathion activation and paraoxon degradation was also observed in the lung preparation, however, this extrahepatic parathion and paraoxon metabolizing activity was not induced by phenobarbital or inhibited by SKF 525-A pretreatment. Phenobarbital pretreatment increased paraoxon level in livers of rats when measured 3 hr following parathion injection (2 mg/kg, ip). SKF 525-A did not alter parathion or paraoxon levels in brain, blood and liver. Phenobarbital pretreatment decreased the toxicity of parathion (4mg/kg, ip) or paraoxon (1.5 mg/kg, ip) as determined by decreases in lethality and inhibition of brain and lung acetylcholinesterases. An additional SKF 525-A treatment failed to decrease the protective effects of phenobarbital against parathion or paraoxon toxicity. These results suggest that some unknown factors other than hepatic MFO induction are involved in the protective action of phenobarbital against parathion and paraoxon toxicity.