• Advances in Traditional Medicine
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• v.9 no.4
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• pp.307-314
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• 2009

Oxidative stress plays an important role in the pathogenesis of various diabetic complications and small intestine is vulnerable to damage resulting in morphological and functional changes. In this study, the effects of Asystasia gangetica leaf extract (AGLE) on oxidative stress status in small intestine of diabetic rats were examined. The leaves of Asystasia gangetica was extracted with 70% ethanol. Oral administration of AGLE once daily (100 mg/kg and 200 mg/kg b.w.) for 28 days to diabetic rats significantly (P < 0.05) increased antioxidant levels of catalase, superoxide dismutase, glutathione peroxidase, glutathione, GSSH, carbohydrate metabolizing enzyme, glucose-6-phosphate dehydrogenase. The increased levels of protein carbonyl content, lipid peroxidation and xanthine oxidase/xanthine dehydrogenase in diabetic rats were reverted back to near normal levels on treatment with AGLE. Both doses of AGLE offered significant activity (P < 0.01) against oxidative damage and were comparable with standard, glibenclamide. The results revealed the occurrence of oxidative stress in small intestine during diabetes and suggest the potential of AGLE as an antioxidant in protecting the tissue defense system against oxidative damage in streptozotocin-induced diabetes.

• Applied Microscopy
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• v.36 no.4
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• pp.291-297
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• 2006

To evaluate the effects of ingestion of alcoholic drinks on the toxicities of industrial compounds, cyclohexane (CH) was intraperitoneally administrated to rats (1.56g/kg body weight), which had been ingested 15% ethanol for up to 6 weeks,4 times by once a day and every other day. Following the last treatment of ethanol or CH, blood and liver tissues were collected after 4 hours prior to sacrifice of animals. By the injection of CH, liver weight (% of body weight) and xanthine oxidase activity in serum were increased, and glucose-6-phasphatase (G6P) activity in liver was decreased compared to them of control group. The activities of CH metabolizing enzymes, such as cytochrome P450 dependent aniline hydroxylase (CYPdAH) and alcohol dehydrogenase (ADH), were significantly increased by injection of CH, and those activities were the highest in CH-injected group after pretreated with alcohol. Ultrastructurally. both of alcohol treatment and CH injection induced transforming into the smooth-endoplasmic reticulum from rough-endoplasmic reticulum, the those rate was the highest in case of CH-injection after pretreated with alcohol. From these results, it is suggested that alcohol intake on a level without alcoholic degeneration of hepatocytes could enhance the CH metabolism of liver.

• The Korean Journal of Pharmacology
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• v.20 no.1 s.34
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• pp.47-54
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• 1984

Effect of ascorbic acid on various hepatic ethanol metabolizing enzymes including alcohol dehydrogenase(ADH), the microsomal . ethanol oxidizing system(MEOS), and catalase was quantitatively evaluated in liver microsomal and cytosolic preparation from Sprague-Dowley rats. In present study, ADH activities were no changed significantly by ascorbic acid. The MEOS activity, dependent on NADPH and $O_2$, was affected by azide (inhibitor of catalase) or exogenous catalase. In the presence of ascorbic acid, ethanol oxidation by rat liver microsomal preparation reacted with NADPH-generating system was increased by up to 22.5%, but decreased when liver microsome was reacted with $H_2O_2$ generated by xanthine and xanthine oxidase. Increase in the activity of the MEOS in the presence of ascorbic acid was greater in liver microsomal preparation pretreated with azide. Also ascorbic acid oxidized ethanol nonenzymatically. This ethanol oxidation induced by ascorbic acid was inhibited by OH radical scavengers (thiourea, sodium benzoate), but was not much affected by superoxide dismutase. From these results it was suggested that ascorbic acidcould interact directly with the MEOS, then promote the oxidation of ethanol. And, to some extent, ${\cdot}OH$-radicals or other radicals generated during the spontaneous autooxidation of ascorbic acid may be responsible for the production of acetaldehyde from ethanol.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1997.04a
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• pp.97-97
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• 1997

It was reported that ATP depletion occurs and accelerates cell damage during ischemia and reperfusion. To determine the mechanism of cell damage, the change of energy metabolism in liver was studied during ischemia/reperfusion. The groups were divided into four categories : sham-operated group, ischemia/reperfusion group, and two types of ATP-MgCl$_2$ treatment groups(one was treated during ischemia and the another during reperfusion). Rats were administered intravenously saline or ATP-MgCl$_2$. Rats were anesthetized and blood vessels in the left and median lobes of the liver were occluded. After 60min of ischemia, the clamp at those vessels were removed. After ischemia, one and five hours after reflow, energy metabolites(ATP, ADP, AMP, inosine, adenosine, hypoxanthine, xanthine) in liver were measured with HPLC. To observe mitochondrial function, aterial keton body ratio in blood and mitochondrial glutamate dehydrogenase activity in liver were measured. And lipid peroxidation was measured to evalutate the involvement of free radicals. In this study, ATP and ADP were catabolized to their metabolites(AMP, inosine, adenosine, hypoxanthine, xanthine) during ischemia and they resynthesized ATP and ADP during reperfusion. But total purine base were not restored to level of normal rat. The main source of resynthesizing ATP and ADP was AMP. In both ATP-MgCl$_2$ treated groups, mitochondrial function was protected and lipid peroxidation was significantly reduced. Our findings suggest that ischemia/reperfusion impairs hepatic energy metabolism.

• Applied Microscopy
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• v.22 no.1
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• pp.113-127
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• 1992

The present study was investigated to elucidate the effects of chlorambucil the heart tissue of various-aged rats. The male rats ranging from 3 to 36 months were used. The cytochemical and biochemical changes in myocardium of the rats were studied in the aspect of free radical roles in aging process. With the goals of evaluating the potential roles of free radicals in aging process, evidence was shought for alterations of myocardial lipid peroxide levels in control and chlorambucil treated rats. The result are summarized as follows: 1. Cytochemical studies showed that the activities of $Mg^{++}$-ATPase and succinic dehydrogenase increased with age. However, these enzyme activities were decreased with treatment of chlorambucil, when compared with control group. Interestingly it was observed that chlorambucil treatment increased the activity of acid phosphatase from 6 months upto 18 months, and decreased after 18 months. 2. The lipid peroxide level in myocatdium was increased with age; chlorambucil-treated group was higher than that of control group. 3. Age-dependent increase in activities of monoamine oxidase, xanthine oxidase and catalase was observed. But the increase of catalase activity was higher than that of monoamine oxidase and xanthine oxidase activity in control group. However, in chlorambucil-treated group, age-dependent decrease of these enzyme activities was observed, and catalase activity was more significant particularly with regard to other enzymes. In consequently, the morphological alterationsof myocardium due to chlorambucil treatment was exclusively observed. We demonstrate that this alteration is occured by lipid peroxidation upon chlorambucil treatment.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.4
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• pp.427-433
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• 1998

In brain hypoxic-ischemia, an excess release of glutamate and a marked production of reactive oxygen species (ROS) occur in neuronal and non-neuronal cells. The present study investigated the effect of the biological antioxidants dihydrolipoic acid (DHLA) and lipoic acid (LA) on N-methyl-D-aspartate (NMDA)- and ROS-induced neurotoxicity in cultured rat cortical neurons. DHLA enhanced NMDA-evoked rises in intracellular calcium concentration ($[Ca^{2+}]_i$). In contrast, LA did not alter the NMDA-evoked calcium responses but decreased after a brief treatment of dithiothreitol (DTT), which possesses a strong reducing potential. Despite the modulation of NMDA receptor-mediated rises in $[Ca^{2+}]_i$, neither DHLA nor LA altered the NMDA receptor-mediated neurotoxicity, as assessed by measuring the amount of lactate dehydrogenase released from dead or injured cells. DHLA, but not LA, prevented the neurotoxicity induced by xanthine/xanthine oxidase-generated superoxide radicals. Both DHLA and LA decreased the glutathione depletion-induced neurotoxicity. The present data may indicate that biological antioxidants DHLA and LA protect neurons from ischemic injuries via scavenging oxygen free radicals rather than modulating the redox modulatory site(s) of NMDA receptor.

• Journal of Life Science
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• v.22 no.1
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• pp.126-131
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• 2012

Physiological activities of hot water (BRW) and 80% ethanol (BRE) extracts from brown rice were investigated in this study. The highest activity (94.9%) of nitrite reductase was observed for BRE at 1 mg/ml at pH 1.2, while the activity for BRW was about 75.4% under the same conditions. The inhibitory effects of BRW and BRE on xanthine oxidase activity were about 39.0 and 72.9% at 10 mg/ml, respectively. The digestibility of starch was lower for brown rice than for milled rice and the highest inhibition (93.1%) of ${\alpha}$-glucosidase activity occurred with BRE. Superoxide dismutase (SOD)-like activities of BRW and BRE were weakly increased in a dose-dependent manner and were about 56.4 and 44.9% at 10 mg/ml, respectively. The influences of BRW and BRE on alcohol metabolizing activity were determined by measuring the generation of reduced nicotinamide adenine dinucleotide (NADH) by alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). Increases in ADH and ALDH activities were only detected with BRE.

• Journal of the Korean Society of Food Science and Nutrition
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• v.26 no.4
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• pp.675-681
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• 1997

This study was conducted to investigate the effect of dietary protein and fiber levels on the activities of ethanol metabolizing enzymes of liver in ethanol-treated rats. Sprague-Dawley male rats were fed on diets containing two levels of protein(7, 20%/kg diet) and pectin(5, 10%/kg diet). In ethanol experiments, ethanol(25% v/v) was administered by oral intubation(5g/kg body weight) at the same time once a day Control animals received an isocaloric dose of sucrose. The rats were sacrificed after 5 weeks of feeding periods. Alcohol dehydrogenase and microsomal ethanol oxidizing system activities of hepatic tissue were increased more in ethanol-treated groups than in control groups. Increment of activities predominated in normal protein normal fiber group. Aldehyde dehydrogenase activity was decreased in ethanol-treated groups and significantly decreased in normal Protein normal fiber group. Cytochrome P-450 content was significantly increased in ethanol-treated groups and Predominated in normal protein groups. Xanthine oxidase activity was increased in ethanol-treated groups, but not significantly except normal protein normal fiber group. Glutathione content tended to increase in proportion to level of dietary protein and was higher in normal fiber groups than in high fiber groups, whereas it was decreased by ethanol treatment. Lipid Peroxide content was significantly increased in low Protein normal fiber groups.

• Preventive Nutrition and Food Science
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• v.3 no.4
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• pp.351-355
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• 1998

The purpose of this study was to investigate the effect of protein and dietary fiber levels on the activities of ehanol metabilizing enzymes of the brain in acute and chronic ethanol-treated rats. Male Sprague-Dwley rats were fed on diets containing two levels of protein(7%, 20%)) with two levels of fiber(5%, 105) for 5 weeks. Rats were orally administered 40% (v/v) ethanol(5g/body weight) 90 min before decapitation in the acute ethanol-treated groups and 25% (v/v) ethanol (5g/kg body weight) once a day for 5 weeks in the chronic ethnol-treated groups. Cytosilic alcohol dehydrogenase (ADH) activities were higher than those of mitochondrial ADH. The ADH activities were increased by 20% protein and %% fiber levels in the diet in two fractions , but were decreased by chronic ethanol treatment. Mitochondrial aldehyde dehydrogenase (ALDH) activities did not change by ethanol treatment but were increased by the 20% protein level. However, cytosilic ALDH activities were decreased by chronic ethanol treatment at the 5% fiber level and did not change with protein levels. Both ALDH activities were higher in the 10% fiber groups than the 5% fiber groups. Cytochrome P-450 contents were significantly increased in the chronic ethanol-treated groups but xanthine oxidase (XO) activities did not change. P-450 contents and XO activities were significantly decreased in both the low protein and fiber groups.

• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.5
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• pp.725-730
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• 1994

This study was conducted to investigate the effect of dietary zinc (Zn) and/or cadmium (Cd) on hepatic microsomal and cytosol enzyme activities. Male Spraque-Dawley rats (110$\pm$10g ) received zinc (0, 30 and 300 ppm/) and Cd-treated groups were administered oral intubation with Cd chloride (5.0mg/kg of body weight 0 at the same time once a week. The effect of Cd on the activity of hepatic cytochromep-450 , xanthine oxidase(X. O) and superoxide dismutase (SOd) was studied in rats. Cd oral intubation resulted in a decrease in cytochrome P-450 content and SOD activity whereas a significant increase in the X.O. activity was observed was observed . Intake of excessive Zn led to an increased activity of microsomal alcohol dehydrogenase (ADH) , whereas Zn deficiency group led to a decreased group. The mechanism by which Zn induces the decreasing of Cd toxicity in rats, seems to rely on the protection of the enzyme systems P-450, ADH, aldehyde dehydrogenase (ALDH) and X.O. in the liver, possibly by forming non-toxic Cd metallothionein. These results indicate that Zn and Cd regulation might occur via inhibitory protein component of the $H_2O$$_2$ -generator system.