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Biomedical subjects

I Ishiguro

Publications and source records attributed to I Ishiguro.

At least 55 records · Page 3Linked to original sources
PubMed1997

Preventive action of vitamin E-containing liposomes on cataractogenesis in young adult rats fed a 25% galactose diet.

The preventive action of vitamin E (Vit. E)-containing liposomes on cataractogenesis was examined in male Wistar rats (five weeks old) fed a 25% galactose diet. Vit. E-containing liposomes prepared with dipalmitoylphosphatidylcholine were instilled into both eyes three times a day over a 45-day period. Cataract appeared at 18-day galactose feeding and developed gradually thereafter. Simultaneous Vit. E-containing liposome instillation delayed this cataractogenesis. Lenses of 18-day galactose-fed rats showed decreases in Vit. E and reduced glutathione (GSH) contents and Na+, K(+)-ATPase activity and increases in lipid peroxide (LPO), galactitol, and water contents. Lenses of 45-day galactose fed rats showed decreases in GSH content and Na+,K(+)-ATPase activity and increases in Vit. E, LPO, galactitol, and water contents. Serum Vit. E and cholesterol levels decreased in 18-day galactose-fed rats, while both levels increased in 45-day galactose-fed rats. Simultaneous Vit. E-containing liposome instillation prevented these changes except for the changes of lenticular galactitol and water contents and serum Vit. E and cholesterol levels. These results indicate that simultaneously instilled Vit. E-containing liposomes can delay cataractogenesis in young adult rats fed a 25% galactose diet mainly by the antioxidative action of Vit. E contained in the instilled liposomes.

Animals↗
PubMed1997

Genetic and biochemical studies on ommochrome genesis in an albino strain of a terrestrial isopod, Armadillidium vulgare.

Genetic studies and quantitative determination of levels of 3-hydroxykynurenine and kynurenine were performed in an albino strain of a terrestrial isopod Armadillidium vulgare. From the results of matings between the albino and the albino, the red, the dark red, or the wild type individuals, the albino A. vulgare seems to be regulated by an autosomal gene(s) recessive to its wild allele. Litter mating of F1 progenies obtained by crossing the albino and the red mutant or the albino and the dark red mutant yielded progenies at a ratio of 3:6:3:4 for the red, the dark red, the wild, and the albino phenotypes, respectively. The albino gene(s) seems not to be allelic but to be epistatic to the red gene(s) with respect to ommochrome biosynthesis. Quantitative determination of 3-hydroxykynurenine carried out by high-performance liquid chromatography with electrochemical detection revealed that the 3-hydroxykynurenine content in the albino was significantly lower than that in the wild or the red type. The whole content of 3-hydroxykynurenine after enzymatic conversion of kynurenine to 3-hydroxykynurenine was still considerably lower than that found in the wild type, even though it increased after the conversion. The albino gene(s) seems to be associated with a blockage at distinct level(s) of ommochrome biosynthesis.

Albinism↗
PubMed1997

Preventive effect of oren-gedoku-to (huanglian-jie-du-tang) extract on progression of carbon tetrachloride-induced acute liver injury in rats.

The effect of oral administration of Oren-gedoku-to (Huanglian-Jie-Du-Tang) extract (TJ-15) on the progression of acute liver injury was examined in rats intoxicated with carbon tetrachloride (CCl4). When TJ-15 at a dose of 500 mg/kg body weight (b.w.) was administered to male Wistar rats aged seven weeks 6 hours after i.p. injection of CCl4 (1.0 ml/kg b.w.), an apparent liver injury occurred. Significant prevention against the progression of liver injury was found 24 hours after the injection judging from the activities of serum transaminases and other indices of liver cell damage. An increase in lipid peroxide level and decreases in reduced glutathione level and superoxide dismutase (SOD) activity occurred in the liver at 6 and 24 hours after CCl4 injection. Serum SOD activity increased 24 hours after CCl4 injection. Post-oral TJ-15 administration significantly ameliorated all these changes found at 24 hours after CCl4 injection. An increase in liver triglyceride level and a decrease in serum triglyceride level also occurred 6 and 24 hours after CCl4 injection. Post-oral TJ-15 administration prevented the increase in liver triglyceride level at 24 hours after CCl4 injection. Although the activity of liver tryptophan 2,3-dioxygenase (TDO), a marker of the inhibition of liver protein synthesis by CCl4, decreased 6 and 24 hours after injection of the toxicant, post-oral TJ-15 administration had no effect on this decrease in TDO activity at 24 hours after the injection. These results indicate that oral TJ-15 administration can prevent the progression of acute liver injury in CCl4-injected rats, and suggest that this prevention could be due to the action of TJ-15 to scavenge free radicals formed in the liver and to inhibit triglyceride accumulation in the liver.

Administration, Oral↗
PubMed1997

Comparative study of oral and parenteral administration of sho-saiko-to (xiao-chaihu-tang) extract on D-galactosamine-induced liver injury in rats.

The preventive effect of Sho-saiko-to (Xiao-Chaihu-Tang) extract (TJ-9) on the progression of D-galactosamine (GaIN)-induced liver injury was examined in five week-old male Wistar rats with oral (p.o.) or intraperitoneal (i.p.) administration of the same dose of TJ-9. Rats treated once with GaIN (500 mg/kg body weight, i.p.) received TJ-9 at a dose of 1.0 g/kg body weight (p.o. or i.p.) 2 hours after GaIN treatment at which time an apparent liver injury occurred. Both p.o. and i.p. administration of TJ-9 showed similar significant prevention against the progression of liver injury 24 hours after GaIN injection. Although total protein and albumin concentrations in serum and protein concentration in the liver decreased with the progression of GaIN-induced liver injury, oral or i.p. administration of TJ-9 prevented these decreases in similar degree. However, decreases in serum and liver triglyceride concentration with the progression of liver injury were not attenuated after p.o. or i.p. administration of TJ-9. The activities of liver 5'-nucleotidase and glucose-6-phosphatase, marker enzymes of liver plasma and microsomal membranes, respectively, decreased during the progression of liver injury. A similar preventive effect on the decrease of both enzyme activities was found after p.o. or i.p. administration of TJ-9. These results indicate that the preventive effect on progression of GaIN-induced liver injury by oral or i.p. administration is approximately equal, and that the effect may be through improving the impaired liver protein synthesis and disrupted liver plasma and microsomal membranes in a similar degree.

5'-Nucleotidase↗
PubMed1997

Involvement of the xanthine-xanthine oxidase system and neutrophils in the development of acute gastric mucosal lesions in rats with water immersion restraint stress.

In rats subjected to water immersion restraint (WIR) stress for 1, 3, and 6 h, gastric mucosal lesions developed time-dependently with an increase in lipid peroxide (LPO) levels and a decrease in nonprotein sulfhydryl levels in the gastric mucosa. The gastric mucosal xanthine oxidase (XO) activity significantly increased with the conversion of xanthine dehydrogenase (XD) to XO at 6 h of WIR (3.2-fold that of the control group without WIR). A significant increase in myeloperoxidase (MPO) activity, an index of neutrophil infiltration, occurred in the gastric mucosa at 3 and 6 h of the WIR (2.2- and 3.3-fold that of the control group without WIR, respectively). In contrast, superoxide dismutase, catalase, and glutathione peroxidase activities in the gastric mucosa did not change during the WIR period. Pretreatment with either allopurinol (AP), an inhibitor of XO, or soybean trypsin inhibitor (STI), a serine protease inhibitor, attenuated the lesion development at 6 h of WIR, but not at 3 h. In the gastric mucosa of rats pretreated with AP, enhancements of LPO formation, sulfhydryl oxidation, and XO activity found at 6 h of WIR were prevented with inhibition of XD plus XO activity, while in the gastric mucosa of rats pretreated with STI, these enhancements were prevented with inhibition of the conversion of XD to XO. In the gastric mucosa of rats pretreated with anti-polymorphonuclear leukocyte antiserum, the lesion development and enhanced LPO formation and sulfhydryl oxidation found at 3 and 6 h of WIR were prevented with a decrease in increased MPO activity. These results indicate that in the gastric mucosa of rats with WIR stress, the progression of lesions is mainly related to enhanced LPO formation and sulfhydryl oxidation which depend on an increased generation of oxygen free radicals via the xanthine-XO system and neutrophils rather than the change in the oxygen free radical-scavenging activity of antioxidant enzymes. The present results also suggest that increased gastric mucosal LPO formation and sulfhydryl oxidation found at 3 h of WIR could be mainly due to neutrophil-derived oxygen free radicals, while enhanced gastric mucosal LPO formation and sulfhydryl oxidation found at 6 h of WIR could be due to both neutrophil- and XO-derived oxygen free radicals.

Allopurinol↗
PubMed1997

Attenuation of disrupted hepatic active oxygen metabolism with the recovery of acute liver injury in rats intoxicated with carbon tetrachloride.

In this study, we examined how disrupted hepatic active oxygen metabolism at a progressed stage of carbon tetrachloride (CCl4)-induced acute liver injury is attenuated with the recovery of the injury in fed rats. When the progression and recovery of liver injury were assessed by measuring the activities of serum transaminases, indexes of liver cell damage, at 2, 24, 48, and 72 h after a single intraperitoneal injection of CCl4 (1.0 ml/kg body weight), an apparent liver injury was found at 2 h, the most progressed liver injury occurred at 24 h, and the progressed liver injury fairly recovered at 72 h. Hepatic superoxide dismutase and catalase activities decreased with the progression of liver injury but both decreases were maintained during the recovery of the injury. Hepatic glutathione peroxidase activity did not change with the progression and recovery of liver injury. Hepatic glutathione reductase activity decreased with the progression of liver injury and the decreased activity was returned up to the original level with the recovery of the injury. Hepatic glucose-6-phosphate dehydrogenase activity increased with the progression and recovery of liver injury but this increased activity was reduced at a late stage of the recovery. Hepatic reduced glutathione and ascorbic acid contents decreased with the progression of liver injury but both decreased contents were returned up to the original levels with the recovery of the injury. Hepatic vitamin E content decreased at an early stage of liver injury but this decreased vitamin E content increased over the original level with the progression of the injury and this increased vitamin E content was maintained during the recovery of the injury. Hepatic lipid peroxide content increased with the progression of liver injury and this increased content was returned near the original level with the recovery of the injury. These results indicate that in rats intoxicated once with CCl4, disrupted hepatic active oxygen metabolism at a progressed stage of liver injury is attenuated with the recovery of the injury mainly through the improvement of hepatic active oxygen metabolism mediated by the glutathione redox cycle and ascorbic acid.

Alanine Transaminase↗
PubMed1996

Conversion of gamma-glutamylcysteinylethyl ester to glutathione in rat hepatocytes.

The conversion of gamma-glutamylcysteinylethyl ester (gamma-GCE) to glutathione in a reduced form (GSH) was examined using isolated rat hepatocytes pretreated with diethylmaleate, a GSH-depletor. Incubation of hepatocytes with 0.1 and 5.0 mM gamma-GCE (gamma-GCE-hepatocytes) over a 30-min period resulted in time-dependent increases in intracellular GSH and nonprotein-SH (NP-SH) concentrations. Hepatocytes incubated with 5.0 mM but not 0.1 mM GSH over a period of 30 min showed a time-dependent increase in intracellular GSH concentration. In the gamma-GCE-hepatocytes pretreated with bis-(p-nitrophenyl)phosphate (BNPP), a non-specific esterase inhibitor, an enhancement of intracellular GSH concentration was markedly reduced. gamma-GCE concentration in the gamma-GCE-hepatocytes with BNPP pretreatment was significantly higher than that in the cells without BNPP pretreatment, although there was no difference in the total amount of intracellular NP-SH, i.e., gamma-GCE, GSH, gamma-glutamylcysteine, cysteine ethyl ester, and cysteine between both gamma-GCE-hepatocytes. The present results indicate that gamma-GCE is transported into liver cells more easily than GSH itself, resulting in its conversion to GSH via esterase and glutathione synthetase within the cells.

Animals↗
PubMed1996

Role of catalase in retinal antioxidant defence system: its comparative study among rabbits, guinea pigs, and rats.

The role of catalase in the retinal antioxidant defence system was examined in rabbits, guinea pigs, and rats with and without prolonged administration of a diet containing 0.4% 3-aminotriazole (3-AT), a catalase inhibitor. When weanling rabbits, guinea pigs, and rats we administered 3-AT for 8, 7, and 10 weeks, respectively, retinal catalase activity was reduced by approximately 50% in all these animals. In the retina of rabbits with 3-AT administration, a decrease in superoxide dismutase (SOD) activity and an increase in lipid peroxide (LPO) concentration occurred. while glutathione peroxidase (GSH-px) activity did not change. In the retina of guinea pigs with 3-AT administration, an increase in LPO concentration occurred, while SOD and GSH-px activities did not change. In the retina of rats with 3-AT administration, a decrease in GSH-px activity and an increase in LPO concentration occurred, while SOD activity did not change. An increase in serum LPO concentration was found in rats with 3-AT administration, while the concentration did not change in rabbits and guinea pigs. These results indicate that catalase plays an important role in the retinal antioxidant defence system, but that the way catalase contributes to the maintenance of the retinal antioxidant defence system is different among these animals. The present results suggest that under the prolonged inhibition of catalase, the retina of rats, but not of rabbits and guinea pigs, may suffer from the influence of systemic oxidative stress.

Amitrole↗
PubMed1996

Anticataract action of vitamin E: its estimation using an in vitro steroid cataract model.

The aim of this study was to estimate the anticataract action of vitamin E using an in vitro methylprednisolone (MP)-induced cataract model. The same severity of early cortical cataract was induced in lenses isolated from male Wistar rats aged 6 weeks by incubation with MP (1.5 mg/ml) in TC-199 medium. The cataractous lenses showed slight increases in lipid peroxide (LPO) content and Na+/K+ ratio and slight decreases in reduced glutathione (GSH) content and glyceraldehyde-3-phosphate dehydrogenase (GAP-DH), a sensitive index of oxidative stress, and Na+,K(+)-ATPase activities. When the cataractous lenses were further incubated in TC-199 medium with and without vitamin E (250 micrograms/ml) for 48 h, the progression of cataract was prevented in the vitamin E-treated lenses, but not in the vitamin E-untreated lenses. The vitamin E-untreated lenses showed a decrease in vitamin E content and an increase in water content in addition to further increases in LPO content and Na+/K+ ratio and further decreases in GSH content and GAP-DH and Na+,K(+)-ATPase activities. In contrast, the changes of these components and enzymes except for GSH were attenuated in the vitamin E-treated lenses. From these results, it can be estimated that vitamin E prevents in vitro cataractogenesis in rat lenses treated with MP by protecting the lenses against oxidative damage and loss of membrane function.

Animals↗
PubMed1996

Involvement of oxidative stress in D-xylose-induced cataractogenesis in cultured rat lenses.

In order to clarify the involvement of oxidative stress in in vitro sugar-induced cataractogenesis, we examined changes in lipid peroxide, reduced glutathione, vitamin E, and water contents following cataractogenesis in rat lenses cultured with 20 mM D-xylose over a period of 24 h. In D-xylose-treated lenses, an apparent opacity appeared at the equator after 6 h of D-xylose treatment, increases in lipid peroxide and water contents and decreases in reduced glutathione and vitamin E contents occurred with the appearance of opacity. We further examined the effect of the treatment of vitamin E in a liposomal form on cataractogenesis and the changes of lipid peroxide, reduced glutathione, vitamin E, water, and xylitol contents in rat lenses cultured with 20 mM D-xylose for 24 h. This vitamin E treatment significantly prevented not only cataractogenesis, but also an increase in lipid peroxide content and a decrease in vitamin E content in the D-xylose-treated lenses. However, the vitamin E treatment had no effect not only on a decrease in reduced glutathione content, but also on increases in water and xylitol contents, which are known to be induced via aldose reductase, in the D-xylose-treated lenses. These results indicate that not only osmotic stress but also oxidative stress should be involved in cataractogenesis in rat lenses cultured with D-xylose and support the involvement of oxidative stress in in vitro sugar-induced cataractogenesis.

Animals↗
PubMed1996

Response of endogenous reduced glutathione through hepatic glutathione redox cycle to enhancement of hepatic lipid peroxidation with the development of acute liver injury in mice intoxicated with carbon tetrachloride.

In the liver of male ddY mice intoxicated once with carbon tetrachloride (CCl4), the change in lipid peroxide (LPO) level with the development of damage over a 24 hr period after i.p. treatment of the toxicant (1.0 mL/kg) was compared with the changes in reduced glutathione (GSH) and oxidized glutathione (GSSG) levels, GSSG/GSH ratio, and activities of the glutathione redox cycle-related enzymes such as Se-dependent glutathione peroxidase (Se-GSH-px), glutathione reductase (GSSG reductase), and glucose-6-phosphate dehydrogenase (G-6-PDH) and of Se-independent glutathione peroxidase (non-Se-GSH-px) with the development of damage during the same period. An apparent liver injury was observed 0.5 hr after CCl4 treatment and the injury progressed rapidly later than 8 hr, judging from the activities of serum transaminases, marker enzymes of liver cell damage. Hepatic LPO level slightly increased once during the first 4 hr after CCl4 treatment and a marked increase in the level occurred later than 12 h, while serum LPO level increased later than 12 h. Hepatic GSH level decreased rapidly during the first 4 hr after CCl4 treatment and the decreased level recovered slowly thereafter, although the recovered level did not reach the control level. Hepatic GSSG level rapidly increased once during the first 1 hr after CCl4 treatment and an increase in the level occurred again later than 12 h. Hepatic GSSG/GSH increased during the first 1 hr and later than 8 hr after CCl4 treatment, although the ratio was maintained above the control level later than 0.5 h. Hepatic Se-GSH-px activity increased during the first 2 hr after CCl4 treatment and later than 8 h, while hepatic non-Se-GSH-px activity increased during the first 1 hr but decreased below the control level at 8 and 12 h. Hepatic GSSG reductase activity decreased during the first 2 hr after CCl4 treatment but the decrease activity returned up to the control level at 8 h. Hepatic G-6-PDH activity increased rapidly during the first 2 hr after CCl4 treatment and the increase proceeded slowly thereafter. These results indicate that although hepatic lipid peroxidation is enhanced at early and progressed stages of liver injury in mice intoxicated once with CCl4, endogenous GSH through hepatic glutathione redox cycle can respond well to enhanced hepatic lipid peroxidation at an early stage of liver injury but not enough to enhanced hepatic lipid peroxidation at a progressed stage of liver injury.

Alanine Transaminase↗
PubMed1995

Preventive effect of dai-saiko-to (da-chai-hu-tang) extract on disrupted hepatic active oxygen metabolism in rats with carbon tetrachloride-induced liver injury.

In order to clarify the preventive action of Dai-Saiko-to (Da-Chai-Hu-Tang) extract (TJ-8) on the progression of acute liver injury in rats intoxicated with carbon tetrachloride (CCl4), we examined the effect of post-oral TJ-8 administration on hepatic active oxygen metabolism following the progression of this liver damage. When TJ-8 (1.0 g/kg body weight) was administered orally to male Wistar rats aged five weeks 2 hrs after i.p. injection of CCl4 (1.0 ml/kg body weight), an apparent liver injury occurred. Significant prevention against the progression of liver injury was found at 24 hrs after injection, judging from the activities of serum transaminases, indexes of liver cell damage. Liver cytosolic superoxide dismutase (SOD) activity decreased 2 and 24 hrs after CCl4 injection, while liver cytosolic catalase and glutathione reductase (GSSG-R) activities decreased 24 hrs after the injection. At 2 and 24 hrs after CCl4 treatment, liver cytosolic Se-containing glutathione peroxidase (GSH-px) activity did not change and liver cytosolic glucose-6-phosphate dehydrogenase (G-6-PDH) activity increased. Post-oral TJ-8 administration significantly ameliorated decreases in liver SOD, catalase, and GSSG-R activities at 24 hrs after CCl4 injection, but did not affect liver Se-GSH-px and increased liver G-6-PDH activities at 24 hrs after the injection. Although increased liver lipid peroxide level and decreased liver reduced glutathione and ascorbic acid levels were observed 2 and 24 hrs after CCl4 injection, post-oral TJ-8 administration significantly prevented these changes found at 24 hrs after injection. These results indicate that post-oral TJ-8 administration can prevent the progression of acute liver injury in CCl4-injected rats by inhibiting enhanced lipid peroxidation and by improving disrupted active oxygen metabolism in the injured liver.

Administration, Oral↗
PubMed1993

Skin L-tryptophan-2,3-dioxygenase and rat hair growth.

We have identified a new enzyme, skin L-tryptophan-2,3-dioxygenase (skin TDO), that catalyzes the degradation of L-tryptophan into formylkynurenine in rats. The rate of this degradation peaks in all rats at 5 to 6 weeks after birth, and also, among rats depilated at 8 weeks old, at 10 to 11 weeks after birth. We have also observed that the properties of this enzyme are closer to those of hepatic L-tryptophan-2,3-dioxygenase (hepatic TDO) than to indoleamine 2,3-dioxygenase. Although an intraperitoneal injection of L-tryptophan increased the activity of skin TDO to approximately 2.2 times greater than control values, an intraperitoneal injection of hydrocortisone and alpha-methyl-DL-tryptophan, both compounds known to affect hepatic TDO activity, had no effect on skin TDO activity. The molecular weight of skin TDO was estimated to be 16.0 kDa, which is close to the molecular weight of hepatic TDO, yet a much larger molecule than indoleamine-2,3-dioxygenase. Increased hair growth rates paralleled increased levels of skin TDO activity in 5- to 6-week-old rats, and marked increases in the activity of skin TDO occurred 2 or 3 weeks after depilation. Enzyme activity was also greatest 2 days before the time of maximum hair root length. Therefore, skin TDO may play an important role in the initiation or suppression of rat hair growth.

Animals↗
PubMed1993

Preparation of glycyrrhetic acid beta-glycosides having beta (1-->2)-linked disaccharides by the use of 2-O-trichloroacetyl-beta-D-pyranosyl chlorides and their cytoprotective effects on hepatic injury in vivo.

Stepwise glycosidation was adopted for the construction of glycyrrhetic acid beta-glycosides (27-30) having beta (1-->2)-linked disaccharides such as 2-O-beta-D-glucuronopyranosyl-beta-D-glucopyranose, 2-O-beta-D-glucuronopyranosyl-beta-D-galactopyranose, 2-O-beta-D-glucopyranosyl-beta-D-glucuronopyranose and 2-O-beta-D-galactopyranosyl-beta-D-glucuronopyranose. In the first glycosidation, 2-O-trichloroacetyl-beta-D-payranosyl chlorides (9-11) were utilized as starting sugar derivatives to react with methyl glycyrrhetinate (5): Glycosidation of 5 with 9 and 10 gave beta- and alpha-monoglycosides (12) and (13), and (15) and (16), respectively. Treatment of the beta-glycosides 12 and 15 with ammonia-saturated ether gave products (14) and (17), respectively. The glycosidation of 5 with 11 followed by treatment with ammonia-saturated ether gave compounds (18) and (19), respectively. The second step glycosidations of 14 and 17 with methyl 2,3,4-tri-O-acetyl-alpha-D-glucuronatopyranosyl bromide (20) gave diglycoside derivatives (23) and (24), respectively, and that of 18 with 2,3,4,6-tetra-O-acetyl-alpha-D-glucopyranosyl bromide (21) and -alpha-D-galactopyranosyl bromide (22) gave diglycoside derivatives (25) and (26), respectively. The removal of the protecting groups of 23-26 gave diglycosides 27-30, respectively, having a beta-D-glucuronopyranose (beta-D-glcUA) as one of two sugar components in the molecules. The cytoprotective effects of the synthesized glycosides 27-30 on carbon tetrachloride (CCl4)-induced hepatotoxicity in vivo were compared with diglycosides 31-33 having only neutral sugar components and naturally occurring glycyrrhizin (34) having two acidic sugar components (beta-D-glcUA).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Preventive effect of gamma-glutamylcysteinylethyl ester on immunological cell injury in isolated rat hepatocytes with anti-rat liver plasma membrane antiserum treatment.

We studied the mechanism by which gamma-glutamylcysteinylethyl ester (gamma-GCE), which is rapidly transported into hepatocytes and converted to reduced glutathione (GSH), prevents immunological hepatic injury. The effect of gamma-GCE on cell injury, as estimated by release of transaminases from cells, and changes in phospholipase A2 (PLA2) activity and of GSH, Ca2+, and lipid peroxide (LPO) contents were examined in isolated rat hepatocytes treated with anti-rat liver plasma membrane rabbit antiserum (ALPMA) and compared with that of GSH. gamma-GCE prevented not only the release of transaminases from hepatocytes treated with ALPMA but also a decrease in GSH content, activation of PLA2, and increases in Ca2+ and LPO contents in the damaged hepatocytes. However, the preventive effect of GSH on these changes was weaker than that of gamma-GCE. In addition, gamma-GCE prevented the development of cell injury in ALPMA-pretreated hepatocytes. These results suggest that gamma-GCE prevents immunological cell injury in ALPMA-treated rat hepatocytes mainly by maintaining the integrity of the plasma membrane through its conversion to GSH within the cells.

Alanine Transaminase↗