The purpose of current study is to investigate the beneficial effect of enzyme (Alcalase) hydrolysates of silk protein in rat. Alcalase-treated silk protein hydrolysate (ATSH) itself did not show any cytotoxicity on the hepatic tissues and blood biochemistry, similar to the normal condition. ATSH played a protective role in tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity and liver damage. The values of AST (aspartate aminotransferase) and ALT (alanine aminotransferase), which are the indicators of the liver function, were effectively alleviated with the ATSH treatment in a dose dependent manner. The level of Lactate dehydrogenase (LDH) and Malondialdehyde (MDA), which were increased with t-BHP treatment, were significantly reduced by ATSH. High dose of ATSH (2 g/kg) reduced the t-BHP-induced LDH release by 48%. Antioxidant and antioxidant enzymes in liver cells were significantly increased by ATSH treatment in their level and activities. ATSH (2 g/kg) increased glutathione (GSH), an intracelluar antioxidant, by 2.5-fold compared with the t-BHP treated group. The activities of glutathione-s-transferase (GST), superoxide dismutase (SOD), and catalase were also elevated by 38%, 60%, and 45%, respectively, with ATSH (2 g/kg) treatment. The antioxidative effect of ATSH was recapitulated to the protection from t-BHP induced liver damages in hematoxylin and eosin (H&E) staining. Thus, ATSH might be used as a hepatoprotective agent.
Inhibitory effects of the methanol extract, hexane extract, methanol soluble fraction (MSF) and juice from 3 weeks fermented Kimchi on the tumor formation in sarcoma-180 cell transplanted mice were studied. Effects of the solvent extracts and juice of the Kimchi on the levels of lipid peroxide, glutathione, and the enzyme activities of the liver were also investigated in normal and sarcoma-180 cell transplanted mice. At 32 days following trans-plantation, MSF reduced the tumor formation by 54% compared with the control group, resulting in the smallest tumor weight. Lipid peroxided content in liver increased by the transplantation of sarcoma-180 cells. However, it decreased when MSF of Kimchi was treated to the mice. MSF also suppressed xanthine oxidase activity in cytosol of the liver cells in mice transplanted by sarcoma-180 cells. Kimchi extracts had no inhibitory effect on hepatic aminopyrine-N-demethylase activity in sarcoma-180 cell transplanted or normal mice. Methanol extract and hexane extract of Kimchi slightly increased hepatic glutathione contents in sarcoma-180 treated mice. The injection of MSF from Kimchi markedly increased glutathione levels in the liver of sarcoma-180 treated mice. The injection of MSF from Kimchi markedly increased glutathione levels in the liver of sarcoma-180 treated mice compared to the controls. The MSF recovered the activities of hepatic glutathione reductase and glutathione S-transferase that decreased by the injection of sarcoma-180 cells. These results showed that MSF of Kimchi could suppress the growth of tumors, inhibiting lipid peroxide production and xanthine oxidase activity, in mice. We also suggested that Kimchi extract might play an important role in the prevention of cancer by enhancement of the glutathione level itself as well as via glutathione reductase and glutathione S-transferase.
We assessed the effect of Se-methylselenocysteine (MSC) treatment, at a dose of 0.75 mg/rat/day for 1 or 2 weeks, on the activities of antioxidant systems in Sprague-Dawley rat tissues. Significant changes in glutathione and antioxidant enzyme activities, with different patterns among tissues, were evidenced. Glutathione content and its reduction state in the liver, lung, and kidney were elevated upon MSC treatment, whereas they were significantly lowered in the spleen. Among the tissues exhibiting glutathione increase, there were different enzymatic responses: $\gamma$-glutamylcysteine ligase activity, the rate-limiting enzyme in the glutathione synthesis pathway, was increased in the liver, whereas the activities of the enzymes associated with glutathione recycling, namely, glutathione peroxidase, glutathione reductase, and glucose 6-phosphate dehydrogenase, were significantly increased in the lung and the kidney. The superoxide dismutase activity was decreased in all tissues upon MSC treatment, whereas catalase activity was increased in all tissues but the liver. Lipid peroxidation level was transiently increased at 1 week in the lung and the kidney, whereas it was persistently increased in the spleen. The increase was not evident in the liver. The results indicate that the MSC treatment results in an increase in the antioxidant capacity of the liver, lung, and kidney principally via an increase in glutathione content and reduction, which appeared to be a result of increased synthesis or recycling of glutathione via tissue-dependent adaptive response to oxidative stress triggered by MSC. The spleen appeared to be very sensitive to oxidative stress, and therefore, the adaptive response could not provide protection against oxidative damage.
Lee Jeong-Won;Lee Song-Shil;Baek Jin-Woong;Lee Sang-Jae;Kim Kwang-Ho
Journal of Society of Preventive Korean Medicine
/
v.8
no.1
/
pp.115-133
/
2004
Hasuohwan(何首烏丸) composed of Polygonum multiflorum Thunb and some medical herbs are known as formula of senescence delay effect. The aim of this study is to investigate the effect of Hasuohwan(何首烏丸) on antioxidant enzyme activity such as Thiobarbituric acid reactive substance(TBARS) in rat plasma and liver, Superoxide dismutase(SOD), Glutathione peroxidase(GSH-px), Catalase(CAT) in rat erythrocyte and liver. Rats were sacrificed and TBARS was measured in rat plasma and liver. SOD, GSH-px and CAT were measured in rat erythrocytes and liver. TBARS in plasma concentrations of HSO group was significantly lower than those of control group. RBC and liver GSH-px activities of HSO group were significantly higher than those of control group. According to above results, it is considered that Hasuohwan is effective in inhibiting lipid peroxidation and increasing antioxidative enzyme activities in D-galactose induced aging rat. Therefore, Hsuohwan is considered in effective of senescence delay.
This work was conducted to investigate the effect of bisphenol A (BPA) on estradiol (E2) 2-and 4-hydroxylase activities in the liver, kidney and lung tissues of male and female rats. After intraperitoneal administration of BPA to male and female rats for 4 days at 0, 10, and 50 mg/kg, the conversion of the substrate for hepatic and extra-hepatic enzyme activities was measured by GC/MSD. The result showed decreases of body and organ weights at 50 mg/kg BPA of male and female rats. Male hepatic E2 2-hydroxylase activity was inhibited by 68% at 10 mg/kg and by 82% at 50 mg/kg BPA. Female hepatic E2 2-hydroxylase activity was decreased by 46% at 10 mg/kg and by 56% at 50 mg/kg to the control. E2 4-hydroxylase was inhibited by 57 and 57% at 10 mg/kg and 54 and 78% at 50 mg/kg in liver of female and male, respectively. The urinary excretion rate of 2-hydroxyestradiol (2-OHE), androsterone and testosterone in urine of female rats with 50 mg/kg BPA were decreased significantly. The results showed that 50 mg/kg BPA was decreased E2 2-and 4-hydroxylase activities in liver, but not in other tissues. The urinary excretion rates of 2-OHE, androsterone and testosterone were also decreased. In liver, estrogenic enzyme activity were higher in male than female. These results suggest that BPA can disrupt estrogen metabolism by suppressing E2 2-and 4-hydroxylase activities in the liver of male and female rats.
This study was undertaken to investigate the effect of lead on organisms. Mice received 15mg or 30mg of lead acetate per kg body weight every day for 1, 2 or 3 weeks, and the livers and kidneys were removed 24h after repeated injections. The livers and kidneys were used as sources for measurement of enzyme activities and for observation of alterations in ultrastructure. It was observed that body weights of mice treated with lead acetate were decreased when compared with those before treatment. This decrease in body weight was proportional to dose. The enzyme activities of succinate and malate dehydrogenases of experimental group that was treated with lead acetate for 1 week were nearly unchanged when compared with controls, but the enzyme activities of experimental group that was treated with lead acetate for 2 or 3 weeks were lower than those of controls. Changes in the enzyme activities were dependent on, but were not proportional to dose. Histologic examination of livers and kidneys after lead treatment showed that lead compound was accumulated and damaged in nucleus and mitochondria mainly. It was also observed that intranuclear inclusion bodies were formed only in epithelial cell of kidney proximal tubule after lead treatment. The overall changes in the ultrastructure were much greater in the livers than in the kidneys. From the above results, it nay be possible to conclude that the lead results in the decrease in body weight, reduction in the succinate dehydrogenate and malate dehydrogenase activities, and damages in the ultrastructure of kidney and liver in mouse. The presence of intranuclear inclusion bodies only in the kidney implies that these bodies protect the kidney from lead toxicity to some extent.
Ninety advanced Catla catla fingerlings (av. wt. 16 g) were randomly distributed in six treatment groups with three replicates each for an experimental period of 60 days to study the effect of dietary lipid source on growth, enzyme activities and immuno-hematological parameters. Six isoprotein (40.0-41.9%) and isocaloric (4,260 kcal $kg^{-1}$) semi-purified diets were prepared with varying levels of soybean oil (SBO) and cod liver oil (CLO) within a total of 8% lipid viz., $D_1$ (Control), $D_2$ (8% SBO), $D_3$ (6% SBO and 2% CLO), $D_4$ (4% SBO and 4% CLO), $D_5$ (2% SBO and 6% CLO) and $D_6$ (8% CLO). Highest SGR was noted in $D_5$ (0.73${\pm}$0.03) group, which was similar with $D_3$ (0.71${\pm}$0.02) and $D_4$ (0.69${\pm}$0.01) groups. Activity of intestinal lipase, hepatic glucose-6-phosphate dehydrogenase (G6PDH) and aspartate amino transferase (AST) of the lipid treatment groups were significantly higher (p<0.05) than the control group. The respiratory burst activity of the phagocytes (Nitroblue tetrazolium (NBT)) was highest in $D_2$ (1.95${\pm}$0.21) followed by $D_3$ (1.19${\pm}$0.15) group, which were significantly (p<0.05) higher than the other groups. Globulin level was significantly higher in $D_3$ (1.29${\pm}$0.08) than in the other groups expect $D_4$. Hemoglobin content and total erythrocyte count did not show any significant difference. From this study, it is concluded that a diet containing 6% soybean oil and 2% cod liver oil ($D_3$) yields higher growth and immune response in Catla catla fingerlings and would be cost effective.
This study investigated the effect of dietary $\beta$-carotene supplementation on lipid peroxidation and anti oxidative enzyme activity as indices of oxidative stress in diabetic rats. Fifty Sprague-Dawley male rats aging 7 weeks were used as experimental animals, which were divided into the non-diabetic control group and the diabetic group. The diabetic group received an intraperitoneal injection with streptozotocin to induce diabetes. Then the diabetic rats were divided into four dietary groups which contained different amounts of $\beta$-carotene; 0%, 0.002%, 0.02%, or 0.2% of the diet. The diabetic rats were fed the experimental diets and the non-diabetic rats were fed the basal diet without $\beta$-carotene supplementation for 2 weeks and then sacrificed. The diabetic group had a significantly higher blood glucose level than the non-diabetic group. However, blood glucose level were not significantly changed by the level of dietary $\beta$-carotene supplementation. Compared to the non-diabetic control group, the diabetic control group indicated a significant increase of plasma thiobarbituric acid reactive substance (TBARS). Liver TBARS level also tended to be higher in diabetic control group, although it was not significant. The $\beta$-carotene supplementation did not reduce plasma TBARS level. However, Liver TBARS level was significantly decreased when 0.02% or more $\beta$-carotene was supplemented in the diet. The liver lipofuscin level in the diabetic control group was higher than in the non-diabetic control group, but the effect of $\beta$-carotene supplementation did not show any differences. Superoxide dismutase activity was significantly lower in the diabetic group, but it was increased in groups receiving 0.02% or more $\beta$-carotene. Compared to the non-diabetic control group, lower activities of catalase and glutathione peroxidase were observed in the diabetic control group, although it was not significant. Catalase and glutathione peroxidase activities tended to increase as the levels of $\beta$-carotene supplementation increased, although it was not statistically significant. Therefore, it seems that dietary $\beta$-carotene supplementation might reduce diabetic complications by partly decreasing the lipid peroxidation and increasing the activity of antioxidative enzyme in diabetes.
Objectives: The aim of this study was to investigate the influence of five herbal medicines on cytochrome P450 (CYP) 3A4 drug-metabolizing enzymes in human liver microsomes. Methods: By using of human liver microsomes, we extracted Cnidium officinale Makino, Rhus verniciflua Stokes, Prunus persica Batsch, Corydalis remota Fisch, Carthamus tinctorius Linne, which are called Hwalhyulgeoouhyak(活血祛瘀藥). Then they were incubated and measured for relative enzyme activity under incubation conditions compared to ketoconazole, which is known as a representative inhibitor of CYP 3A4. Results: We showed that all of five traditional herbal medicines had no inhibition effect of CYP 3A4 at 10, 20, 30, 40, and 50${\mu}g/m{\ell}$ doses in human liver microsomes, although Rhus verniciflua Stokes (RVS) showed a little inhibition as about 95% enzyme activity of control. However, this result was not enough to prove that RVS has a CYP 3A4 inhibition effect. Moreover, we can't confirm that those rates have significant induction effect on CYP 3A4. Conclusions: The result of this study could support that those herbal medicines are more reliable than chemical drugs, even if this is a basic step to prove that result.
This paper examines the effects of dietary fats on the fatty acid composition and market enzyme activites during liver damage in 2-acetylaminofluorene treated rats. Weaning Sprague-Dawley male rats were fed the diet of beef tallow(BT source of sturated fatty acid) corn oil(CO source of n-6 fatty acid) and perilla oil(PO source of n-3 fatty acid) at the level of 15% fat. Ten days after feeding 2-acetylaminofluorene(2-AAF) was injected intraperitoneally twice every week at the level of 50mg/kg body weight for 7 weeks. Liver microsomal and cytosolic fractions were collected to determine the microsomal fatty acid composition lipid peroxide(malondialdehyde MDA) contents glucose 6-phosphatase(G6 Pase) activity cytochrome(Cyt) P-450 contents and cytosolic glutathione S-transferase(G6 Pase) activity cytochrome(Cyt) P-450 contents and cytosolic glutathione S-transferase(GST) activity. The fatty acid composition in microsomal fraction was reflected by different dietary fats. By 2-AAF treatment linoleic acids were increased regardless of the diet MDA contents were higher in CO group than it was in BT group. However 2-AAF treatment decreased MDA contents in all dietary groups. G6Pase activity of BT group was higher than those of the other gropus. CO group had the highest Cyt P-450 contents and 2-AAF treatment lowered Cyt P-450 contents only in CO gropu GST activites were higher in CO than in BT group whereas the enzyme activites were increased by 20AAF treatment in all dietary groups. These results suggest that dietary fats and 2-AAF treatment in all dietary groups,. These results suggest that dietary fats and 2-AAF treatment affect microsomal fatty acid composition The enzyme activities concerned with liver damage were influenced differently by dietary fats and 2-AFF treatment Although PO diet contains much more polyunsaturated fatty acids than CO diet PO diet doesn't cause more oxidant stress compared with CO diet in these data.
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