Purpose: To study temporal pattern of serum liver enzymes levels in newborns with hepatic injury associated with birth asphyxia (BA). Methods: Singleton term newborns with BA and ${\leq}72$ hours of age admitted to neonatal intensive care unit were prospectively enrolled. Term newborns with physiological jaundice and without BA were studied as controls. Serum liver enzymes were measured at <24 hours, 24-72 hours, and at 6-12 days of age for cases and at 1-6 days of age for controls. BA was defined by 1 minute Apgar score <7 or delayed or absent cry with hypoxic ischemic encephalopathy. BA-associated liver injury was defined as serum alanine aminotransferase (ALT) elevation beyond +2 standard deviation (ALT > +2 SD) above the mean of control subjects at any of the three time points. Results: Sixty controls and 62 cases were enrolled. Thirty-five cases (56%) developed BA-associated liver injury (ALT>81 IU/L). They had higher serum levels of ALT, aspartate aminotransferase, lactate dehydrogenase than the control infants, with peak at 24-72 hours. In controls, serum liver enzyme levels were significantly higher in appropriate-for-date (AFD) babies than small-for-date (SFD) babies. Serum enzyme pattern and extent of elevation were comparable between SFD and AFD babies. Degree of serum liver enzyme elevation had no relationship with severity of hypoxic encephalopathy. Conclusion: Serum liver enzyme elevation is common in BA; it peaks at 24-72 hours followed by a sharp decline by 6-12 days of age. Pattern and extent of enzyme elevation are comparable between SFD and AFD babies.
The effect of bear bile on 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD)-induced hepatotoxicity was investigated in 6-week-old C57BL/6 male mice. Bear bile (100 mg/kg or 500 mg/kg) was administered orally daily for 4 weeks, respectively. From the second week, $10\;{\mu}g/kg$ of TCDD was administered to the bear bile-treated animals orally once a week for 3 weeks (a total of $30\;{\mu}g/kg$). There were no specific clinical findings and significant body weight changes in all groups. Although the livers in TCDD-treated mice appeared a severe hypertrophy and many necrotic foci, and changed to yellow-brown color in gross findings, these lesions were remarkably reduced by bear bile administration. The elevated serum activities of alanine transaminase, aspartate transaminase, alkaline phosphatase, and lactate dehydrogenase due to TCDD were significantly decreased by bear bile treatment (P<0.05). The lipid peroxidation induced by TCDD was significantly prevented by bear bile administration (P<0.05). In histological examinations, there were a moderate necrosis of hepatic cells around central veins, severe cytoplasmic vacuolizations, inflammatory cell infiltrations, and remarkable fatty changes in the liver of TCDD-treated animals. However, the lesions were dose-dependently inhibited by the bear bile treatments. These findings indicate that bear bile may have a protective effect against TCDD-induced hepatotoxicity in mice.
We investigated the effects of healthful decoction utilizing Phellinus linteus(HDPL) for suppression in the process of carbon tetrachloride (CCl₄4)-induced inflammation(50% CCl₄ : olive oil=1:1, 1 ㎖/KgㆍB.W.) of rat using biochemical, Western, histological and immunohistochemical analysis. Biochemical analysis of serum showed that the level of aspartate aminotransferase, alanine aminotransferase, lactate Dehydrogenase, alkaline phosphatase and triglyceride were significantly decreased by pretreatment of HDPL, but albumin and nitric oxide were increased. Immunoblot analysis of the liver showed that CCl₄-induced expression of interleukin-1β(IL-1β) and inducible nitric oxide synthase(iNOS) was inhibited by pretreatment of HDPL. More severe histopathological changes of the liver such as Kupffer cell reaction, inflammatory cell infiltration and focal necrosis were demonstrated in the rats challenged with CCl₄ compared with normal. Fewer scores of these changes were observed in the HDPL pretreated rats. Immunohistochemical analysis of the liver showed that while the expression of IL-1β, iNOS, tumor necrosis factor-α, COX(cyclooxygenase)-1 and COX-2 tended to increase, a decline of these immunoreaction of HDPL pre-treated groups were observed in the hepatocytes, especially in the focal necrotic sites. These results suggest that HDPL may act as a therapeutic agent for liver disease through a regulation of inflammation-related proteins.
Crataegii Fructus is commonly used as a improving digestion, removing retention of food, promoting blood circulation and resolving blood stasis agent in East Asia. Cadmium (Cd) is widely distributed in the environment due to its use in industry. An exposure to Cd causes dysuria, polyuria, chest pain, hepatic and renal tubular diseases. The liver is the most important target organ when considering Cd-induced toxicity because Cd primarily accumulates in the liver. This study investigated the protective effect of Crataegii Fructus water extract against cadmium ($CdCl_2$, Cd)-induced liver toxicity in H4IIE cells, a rat hepatocyte-derived cell line and in rats. Cell viability was significantly reduced in Cd-treated H4IIE cells in a time and concentration-dependent manner. However, Crataegii Fructus water extract (CFE) protected the cells from Cd-induced cytotoxicity via inhibition of PARP cleavage. To induce acute toxicity in rats, Cd (4 mg/kg body weight) was dissolved in normal saline and intravenously injected into rats. The rats then received either a vehicle or silymarin (as a positive control) or CFE (50, 100 mg/kg/day) for 3 days, and were subsequently exposed to a single injection of Cd. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were significantly increased by Cd treatment. In contrast, pretreatment with CFE reduced ALT, AST and LDH. In histopathological analysis, CFE reduced the hepatic degenerative regions and the number of degenerative hepatocytes. These are considered as direct evidences that Crataegii Fructus has favorable inhibitory effects on the Cd-intoxicated liver damages. The efficacy of Crataegii Fructus shows slight lower than that of silymarin in the present study.
The present work is aimed to evaluate the protective effect of glutathione-enriched Saccharomyces cerevisiae FF-8 strain on carbon tetrachloride ($CCl_4$)-induced hepatotoxicity and oxidative stress in rats. The activities of liver markers (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase), lipid peroxidative index (thiobarbituric acid-reactive substances), and the antioxidant status (reduced glutathione) were used to monitor those protective roles of FF-8 strain. The liver marker enzymes in plasma and the lipid peroxidation in the liver were increased when $CCl_4$ was treated but these were significantly decreased by FF-8 strain treatment. The hepatic concentration of glutathione in the current glutathione-enriched FF-8 strain fed animal was approximately twice as high as the normal, but this was slightly increased in response to $CCl_4$ plus glutathione-enriched FF-8 strain. The increased liver triglyceride concentration due to the $CCl_4$ treatment was significantly decreased by FF-8 strain and the reduced level reached to that of normal group. Administration of FF-8 strain in normal rat did not show any signs of harmful effects. Therefore, the current findings suggest that FF-8 strain could be an effective antioxidant with no or negligible side-effects and it might be useful for the purpose of protection treatment of hepatotoxicity and oxidative stress in $CCl_4$-treatment in rat.
It is noted that Dioscorea quinqueloba is a medicinal herb that is widely used to treat cardiovascular disease and is assessed as useful to treat other various medical conditions. The immunopotentiating effects of the protein extract (DQP-1) from Dioscorea quinqueloba were thus formally investigated in vivo under incident of cold stress. In this case study, the spleen and thymus weight in mice was shown to have decreased after a measured exposure to cold stress, while the adrenal gland weight in the mice was shown to have increased. The systematic oral administration of DQP-1 significantly recovered the weight loss of the spleen and suppressed the adrenal gland hypertrophy during the association with cold stress. Additionally, the DQP-1 also restored the ascorbic acid level in the adrenal gland reduced after cold stress. The cold stress exposure lowered the percentage of $CD4^+$ and $CD8^+$ cells in the mouse thymus as determined by the flow cytometric analysis, as well as the levels of some serum immunological cytokines(interleukin-2, interleukin-12, and interferon-${\gamma}$) in the studied mice. The resulting identified weakened immunity caused by cold stress was also recovered by a treatment with DQP-1. The DQP-1 significantly suppressed the formation of serum enzymes of alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase, which were systematically elevated during the cold stress episode. These results indicate that DQP-1 can improve immunity in mice that are characteristically weakened under stress.
Park, In-Ho;Hwang, Moon-Young;Woo, Jae-Suk;Jung, Jin-Sup;Kim, Yong-Keun
The Korean Journal of Physiology and Pharmacology
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제3권5호
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pp.529-538
/
1999
This study was undertaken to examine the effect of ethanol on $Na^+ -dependent$ phosphate $(Na^+-P_i)$ uptake in opossum kidney (OK) cells, an established renal proximal tubular cell line. Ethanol inhibited ^Na^+-dependent$ component of phosphate uptake in a dose-dependent manner with $I_{50}$ of 8.4%, but it did not affect $Na^+-independent$ component. Similarly, ethanol inhibited $Na^+-dependent$ uptakes of glucose and amino acids (AIB, glycine, alanine, and leucine). Microsomal $Na^+-K^+-ATPase$ activity was not significantly altered when cells were treated with 8% ethanol. Kinetic analysis showed that ethanol increased $K_m$ without a change in $V_{max}$ of $Na^+-P_i$ uptake. Inhibitory effect of n-alcohols on $Na^+-P_i$ uptake was dependent on the length of the hydrocarbon chain, and it resulted from the binding of one molecule of alcohol, as indicated by the Hill coefficient (n) of 0.8-1.04. Catalase significantly prevented the inhibition, but superoxide dismutase and hydroxyl radical scavengers did not alter the ethanol effect. A potent antioxidant DPPD and iron chelators did not prevent the inhibition. Pyrazole, an inhibitor of alcohol dehydrogenase, did not attenuate ethanol-induced inhibition of $Na^+-P_i$ uptake, but it prevented ethanol-induced cell death. These results suggest that ethanol may inhibit $Na^+-P_i$ uptake through a direct action on the carrier protein, although the transport system is affected by alterations in the lipid environment of the membrane.
Objective: In this study, the effects of saffron stigma against subacute diazinon (DZN) toxicity on enzymes levels, biochemical, hematological, histopathological and genotoxicity indices were studied in rats. Methods: Vitamin E (200 IU/kg) and the aqueous extract of saffron (50, 100 and 200 mg/kg) were injected intraperitoneally three times per week alone or with DZN (20 mg/kg/day, orally) for 4 weeks. The hematological and biochemical parameters were evaluated at the end of 4 weeks. Results: Reticulocytes counts, alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatine phosphokinase, CPK-MB, gama glutamyl transferase (GGT), uric acid and micronucleus indices were increased significantly but total protein and RBC cholinesterase activity were decreased in the DZN-treated group. Saffron prevented the effect of DZN on GGT (50 mg/kg), LDH, CPK and CPK-MB (100 and 200 mg/kg) levels. An increased uric acid and reduced protein levels by DZN were prevented by vitamin E and some doses of saffron. A significant reduction was observed in platelets, RBC, hemoglobin and hematocrit indices in the DZN group. Saffron and vitamin E prevented this reduction. Vitamin E and saffron did not reduce the effect of DZN on RBC cholinesterase activity. The extract and vitamin E could not prevent DZN genotoxicity in the micronucleus assay. Other biochemical parameters and pathological evaluation did not show any abnormality in tissues of all groups. Conclusion: This study shows that vitamin E and saffron reduce DZN induced hematological and biochemical toxicity. However, they do not prevent the genotoxicity induced by DZN.
A laboratory experiment was conducted to determine chronic effects of waterborne copper exposure on rock bream Oplegnathus fasciatus using a panel of enzymes. The activities of the following biochemical biomarkers were determined at different concentrations of $CuSO_4$ for 10 and 20 days: alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) in plasma; antioxidant enzymes including glutathione (GSH), superoxide dismutase (SOD) and glutathione peroxidase (GPx) in liver and gills; and acethylcholinesterase (AChE) in brain and muscle. After exposure to two $CuSO_4$ concentrations (200 and $400{\mu}g/L$), the activities of plasma ALT in the fish showed a tendency to increase with AST and LDH, depending on $CuSO_4$ concentration. Additionally, GSH levels and SOD activities significantly increased, depending on $CuSO_4$ concentrations in liver and gills. This involved the inactivation of reactive molecules formed during oxidative stress, which could provide protection against oxidative damage induced by $CuSO_4$. However, GPx and AChE activities significantly decreased with $CuSO_4$ in liver and gills. In conclusion, these enzymes may represent convenient biomarkers for monitoring heavy metal pollution in coastal areas. Such chronic exposure studies are necessary for improving our understanding of complementary or deleterious effects of pollutants, and for developing metal toxicity biomarkers.
Adebayo, Joseph Oluwatope;Adewumi, Olumuyiwa Sunday;Baruwa, Simbiat Titilayo;Balogun, Elizabeth Abidemi;Malomo, Sylvia Orume;Olatunji, Lawrence Aderemi;Soladoye, Ayodele Olufemi
셀메드
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제6권2호
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pp.12.1-12.7
/
2016
Cocos nucifera (C. nucifera) oil is indigenously used to treat cardiovascular diseases. However, coconut husk fibre (which is rich in polyphenols) has not been screened for this property. Based on the ethnomedicinal use of polyphenols in treating cardiovascular diseases, this study was carried out to evaluate the effects of polyphenols of C. nucifera husk fibre on selected cardiovascular disease indices in mice. Fifty adult male Swiss albino mice were assigned randomly into five groups (A-E). Mice in groups B, C, D and E were administered 31.25, 62.5, 125, and 250 mg/kg body weight polyphenols of ethyl acetate extract of C. nucifera husk fibre respectively while the control group (A) mice received 5% DMSO for seven days. The mice were sacrificed twenty four hours after the last administration of polyphenols. Heart and plasma lactate dehydrogenase (LDH), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) activities and plasma lipid profile were determined. Results revealed significant reduction (*p< 0.05) in plasma levels of total cholesterol and LDL-cholesterol with no significant change (*p> 0.05) in HDL-cholesterol, triglyceride and VLDL levels in the plasma at all doses of polyphenols administered compared to controls. There was significant reduction (*p< 0.05) in the activities of heart AST and LDH while plasma ALT, AST, and ALP activities were not significantly altered (*p> 0.05) at all doses of polyphenols administered compared to controls. These results suggest that the polyphenols of C. nucifera husk fibre possess cardio-protective properties and also indicate their possible use in the treatment of cardiovascular diseases.
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