Serum Liver Marker Enzymes Research Articles

Acute Toxicity and Hepatocurative Effect of Aqueous Leaf Extract of Jatropha curcas in Rats

Acute toxicity and effect of aqueous leaf extract of Jatropha curcas (ALEOJC) on carbon tetrachloride (CCl 4) induced hepatotoxicity in albino rats was evaluated. The rats (60) were divided into five groups designated as; I, II, III, IV and Vof which groups I and II has 15 rats each while, group III, IV and V have 10 rats each. Groups II to V were induced with hepato-toxicity using 150 mg/kg body weight CCl 4 intramuscularly. Serum liver marker enzymes were assayed 48hrs after induction of liver injury followed by 2 nd and 4 th weeksof treatment with ALEOJC and Livolin. Oral LD 50 of ALEOJC was found to be 2,792.85 mg/kg. Serum levels of alanine amino transferase (ALT), Aspartate amino transferase (AST), Alkaline Phosphatase (ALP) and bilirubin level were significantly (P<0.05) increased in group II (untreated rats) compared to group I (normal control). Following treatment with ALEOJC {10 mg/kg (Group III) and 1000 mg/kg (Group IV)} orally, once daily for 4 weeks, a significant hepatocurative effect was observed as evident by decreased level of the serum liver marker enzymes, total bilirubin and direct bilirubin and increase in serum albumin. The hepatocurative effect of ALEOJC is comparable to the standard drug livolin (Group V

Comparative Effects of Ethanolic Extract of Gongronema latifolium and Piper guineense on Blood Electrolytes in Ethanol Exposed Wistar Rats

Aim: The effects of ethanolic extract of Gonngronema latifolium and Piper guineense on serum electrolytes, function indices and liver marker enzymes on wistar rats exposed with ethanol were investigated. Methology: Forty male albino rats (weighing 150-220 g) were used. The animals were divided into four groups A, B, C, and D with C and D subdivided into four subgroups; C1, C2, C3 and C4; D1, D2, D3 and D4 for G. latifolium and Piper guineense respectively, each contained four rats. Group B, and sub groups C and D rats were exposed with 70% ethanol for 7 days to induce liver damage and later treated group C and D with ethanol extracts for 21 days. The following quantities were administered orally to the albino rat per kg body weight: 200, 400,600, and 800 mg; while 0.9% normal saline was served to both the control group. The levels of serum electrolytes and liver marker enzymes were monitored in order to evaluate the protective effects of the plant extracts. The blood was collected through cardiac puncture under chloroform anesthesia after 21 days. Thereafter, the sera were analyzed to determine the status of selected blood electrolytes: sodium (Na+), potassium, (K+), calcium, zinc, bicarbonate, and biochemical indices ALT, AST, ALP and total bilirubin levels. Results: The results showed that the level biochemical indices increased significantly (p<0.05) whereas electrolytes, in negative control were significantly (p<0.05) reduced compared to positive control and treated groups. A significant increase (p<0.05 ) in Na, K, Zn, Ca, and HCO2 in ethanol exposed and treated groups attaining near normalization in a dose - dependent fashion in both G. latifolium and Piper guineense after 21 days therapy were observed. These results highlight the ability of Gongronema latifolium at high doses and Piper guineense at lower doses to ameliorate electrolytes imbalance in wistar rats exposed to ethanol by reducing liver markers towards normal and the observed effects are associated with their antioxidant activities.

Fenugreek seed extract and its phytocompounds- trigonelline and diosgenin arbitrate their hepatoprotective effects through attenuation of endoplasmic reticulum stress and oxidative stress in type 2 diabetic rats

Fenugreek seed and some of its phytoconstituents are known to possess hypoglycemic and hypolipidemic properties but their mode of action in insulin target tissues remains to be elucidated. As hepatic insulin resistance contributes to the development of type 2 diabetes mellitus (T2DM), the protective effects of fenugreek seed extract (FSE) and two of its phytoconstituents-trigonelline and diosgenin were evaluated in T2DM rats with special focus on changes in endoplasmic reticulum (ER) stress and oxidative stress markers in liver. Trigonelline and diosgenin content in FSE were quantified by HPTLC. T2DM was induced in male Sprague–Dawley rats by feeding high-fat diet and administration of low-dose streptozotocin. T2DM rats exhibited hyperglycemia and significantly reduced serum C-peptide levels. Liver damage in T2DM rats was marked by significantly elevated levels of liver marker enzymes in serum, liver triglycerides (TGs), and reduced liver glycogen and was further confirmed by histological analysis. T2DM rats also displayed twofold–threefold increase in the levels of ER chaperones Bip, protein disulfide isomerase (PDI) as well as ER stress associated proapoptotic markers CHOP, Caspase12 and Caspase3 in liver along with elevated lipid peroxidation (LPO) and reduced antioxidant levels. Promisingly, FSE, trigonelline, and diosgenin were found to exhibit protective effects individually and brought about significant reduction in serum enzymes, liver TGs, LPO, expression of liver ER stress marker proteins, and significant increase in liver glycogen content and antioxidants. Histological analysis also supported their protective effects suggesting that FSE and its phytoconstituents alleviate T2DM associated liver damage by normalizing ER stress and oxidative stress.

Lycopene modulates initiation of N-nitrosodiethylamine induced hepatocarcinogenesis: Studies on chromosomal abnormalities, membrane fluidity and antioxidant defense system

Oxidative damage due to free radicals generated during nitrosamine metabolism has been suggested as one of the major cause for the initiation of hepatocarcinogenesis. Lycopene, is a well known antioxidant and have promising preventive potentials, however the mechanism of action remain hypothetical and unclear. To investigate the involvement of lycopene extracted from tomatoes (LycT) against oxidative stress induced deleterious effect of N-nitrosodiethylamine (NDEA) on cellular macromolecules, female Balb/c mice were divided in four groups: Control, NDEA (cumulative dose of 200mg NDEA/kg body weight injected intraperitoneally in 8weeks), LycT (5mg/kg body weight given orally on alternate days, throughout the study) and LycT+NDEA (co-administration of LycT and NDEA). NDEA treatment commenced after 2 weeks of LycT administration. At the end of NDEA exposure i.e., at 10th week, enhanced activities of hepatic phase I enzymes, levels of reactive oxygen species (ROS), lipid peroxidation (LPO) was observed in NDEA group which may have contributed in chromosomal aberrations, enhanced micronucleated cell score, membrane fluidity and serum liver marker enzymes. A significant decrease in enzymatic and non-enzymatic antioxidant system could delineate the mechanism behind such NDEA insults. LycT pre-treatment to NDEA challenged group showed lower chromosomal abnormalities, micronucleated cells score, ROS, LPO levels and liver enzymes. Lycopene aids in normalizing the membrane fluidity and enhancing the activity of antioxidant enzymes and reduced glutathione which could account for the reduced oxidative damage in LycT+NDEA group. It seemed that lycopene supplementation target multiple dys-regulated pathways during initiation of carcinogenesis. Thus, dietary supplementation with lycopene can serve as an alternate measure to intervene the initiation of carcinogenesis.

Cinnamon modulates biochemical alterations in rats loaded with acute restraint stress

The present study was undertaken to investigate pretreatment efficacy of cinnamon (Cinnamomum zeylanicum) on blood glucose level as well as oxidative changes at the liver level.Following acute restraint stress, the experimental animals (n=6) were randomly assigned into four groups, i.e., non-stressed control, stress control and treatment groups (cinnamon decoction 10%, 3 and 6ml/kg, p.o, for 7days). Anti-stress effect of cinnamon was studied by estimation of blood glucose level, liver marker enzymes; aspartate amino transferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and lactate dehydrogenase, liver reduced glutathione (GSH) and liver antioxidant enzymes; super oxide dismutase (SOD), glutathione-S-transferase (GST), catalase (CAT) and glutathione reductase (GR). Acute restraint stress was evidenced by reduction of blood glucose level and liver GSH and elevation of liver marker enzymes in serum. In addition, antioxidant enzymes were drastically inhibited in liver homogenate of stress control rats. Pre-treatment with cinnamon decoction 10%, (3ml/kg and 6ml/kg, p.o, for 7days) avoided the changes observed in stress control rats. This study substantiates that cinnamon is effective in minimizing stress responses thereby beneficial in stress therapy.

Potential chemopreventive role of chrysin against N-nitrosodiethylamine-induced hepatocellular carcinoma in rats

Chrysin is a naturally occurring biological compound, found in honey, propolis and in many plants showing anticancer, anti-inflammation and antioxidant properties. In the present study we focused mainly on the chemopreventive effects of chrysin against N-nitrosodiethylamine-induced hepatocellular carcinoma in Wistar albino by assessing the levels of tumour markers, serum liver marker enzymes, oxidative stress indices, histopathological changes and expressions of proliferating cell nuclear antigen. Significant increases in liver weight, liver marker enzymes such as transaminases, gamma glutamyl transpeptidase, lactate dehydrogenase, 5′ nucleotidase were observed in rats with N-nitrosodiethylamine-induced hepatocellular carcinoma. Animal treated with chrysin shows attenuation of biochemical and histological changes significantly when compared to N-nitrosodiethylamine-induced animals. Alpha-feto protein and carcino embryogenic antigen are well-known tumour markers and their levels were significantly increased in rats with N-nitrosodiethylamine-induced hepatocellular carcinoma and these levels reduced markedly with chrysin treatment. Chemopreventive effect of chrysin further confirmed by observing the histopathological changes, proliferating cell nuclear antigen expressions by western blotting analysis. Restoration of the normal architecture of liver tissue and decreased proliferating cell nuclear antigen and tumor marker expressions were observed in chrysin treated animal groups. With confining these data, the chemopreventive role of chrysin has been well established against N-nitrosodiethylamine-induced hepatocellular carcinoma.

Protective role of propolis against reproductive toxicity of chlorpyrifos in male rats

Chlorpyrifos (CPF) is causing different toxicity and propolis has been reported to be an effective antioxidant. Therefore, the present study is aimed to elucidate the possible protective effects of propolis in alleviating the toxicity of chlorpyrifos on reproductive performance, testosterone levels, enzyme activities and lipids profile in serum of male rats. Animals were divided into four groups; one orally administered (o.d.) CPF at a dose of 9 mg/kg b.w. for consecutive 70-days, propolis group (50 mg/kg b.w.), propolis and chlorpyrifos group and a control group. Results showed that there was a correlation between CPF administration and the significant decrease of the sperm counts, spermatozoon survival and testosterone level as well as increase of sperm aberrations. CPF increased significantly the lipid profile and the levels of various serum liver marker enzymes. In contrast, co-administration of propolis to CPF-treated rats restored almost most of these biochemical parameters to normal levels. On the other hand, CPF resulted in histopathological alterations in testes of male rats. However, pre-administration of propolis to CPF-treated animals improved the testicular damage and alleviates the toxic effects of CPF on reproductive functions in male rats.

English

Avocado,&nbsp;Persea americana&nbsp;Mill. (Lauraceae) is a widely consumed fruit in many countries for its nutritional and medicinal benefits. In the present study, avocado fruit pulp (AFP) was investigated for its anti-hyperlipidemic and antioxidant activities in Wistar albino rats. Hyperlipidemia in the animal was induced by feeding high cholesterol diet (HCD) for 70 days in standard chow diet. Rats on HCD showed significant increase in serum liver marker enzymes (GOT, GPT, GGT, ALP) and bilirubin levels; cholesterol, increased low density lipoprotein cholesterol (LDL-C), very low density lipoprotein cholesterol (VLDL-C) and triglycerides (TG) levels in serum were also elevated. Besides, an increase in lipid peroxidative indicator malondialdehyde (MDA) level, there was a decrease in serum HDL-C; non-protein sulfhydryl (NP-SH) and total protein (TP) in both liver and heart tissues. Treatment with AFP (1 and 2 ml/rat/day, orally) showed significant decrease in serum cholesterol, LDL-C, VLDL-C, TG, glutamic-pyruvic transaminase (GPT), glutamic-oxaloacetic transaminase (GOT),&nbsp;g-glutamyl transpeptidase (GGT)&lrm;, alkaline phosphatase (ALP) and bilirubin levels, while liver and heart MDA was also significantly decreased. After ingestion of AFP, significant increase in non-protein sulfhydryl (NP-SH), total protein (TP) contents in both tissues were observed. Assessment of liver and heart pathology showed that AFP administration caused an improvement in fatty acid changes of the tissues caused by&nbsp;heavy-chain disease (HCD). These results suggest that AFP possesses hypocholesterolemic and antioxidant properties due to its phytoconstituents contents and substantiates its use in folkloric practices to control dyslipidemia. &nbsp; Key words:&nbsp;Avocado,&nbsp;Persea Americana, hypolipidemia, anti-oxidant.

Baicalin prevents cadmium induced hepatic cytotoxicity, oxidative stress and histomorphometric alterations

Therapeutic potential of baicalin was evaluated against Cd-induced hepatic cytotoxicity and oxidative stress. Exposure to Cd (cadmium chloride) in Chang liver cell culture produced cytotoxicity in terms of increase in cell growth inhibition rate, alanine aminotransferase, lactate dehydrogenase, and cellular lipid peroxidation, which was significantly mitigated by baicalin in a concentration dependent manner. Acute exposure to Cd (6.5 mg/kg body weight; ip once only) produced a condition of oxidative stress in rats and substantially increased LPO and GSSG level along with corresponding decrease in GSH and various antioxidant enzymes in liver and also increased the leakage of liver marker enzymes in serum. Therapy with baicalin after 3 h of Cd administration inhibited LPO and formation of GSSG along with increase in liver GSH level. Release of serum transaminases, alkaline phosphatase and lactate dehydrogenase were significantly restored towards control after baicalin treatment. Administration of baicalin helped in restoring the activities of antioxidants enzymes, i.e., superoxide dismutase, catalase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase towards control. Histomorphometric analysis also supported biochemical findings of the study. The observations clearly demonstrated that baicalin treatment ameliorated Cd induced hepatic cytotoxicity and oxidative stress and provides evidence for its therapeutic potential against Cd induced oxidative stress.

Protective effect of kombucha tea against acetaminophen-induced hepatotoxicity in mice: a biochemical and histopathological study

Acetaminophen overdose causes severe hepatotoxicity leading to liver failure in experimental animals and humans. This study was undertaken to evaluate the protective effect of kombucha tea (KT) against acetaminophen-induced hepatotoxicity. Forty male Balb/c mice were divided into four equal groups: (1) the control group, (2) KT-treated group, (3) acetaminophen-treated group, and (4) KT/acetaminophen-treated group. All mice in group 4 were given KT orally for 7 days before a single hepatotoxic dose of acetaminophen (1,000 mg/kg orally). Activities of liver marker enzymes in serum; aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP); and total protein (TP), albumin (ALB), and direct and total bilirubin levels were determined. Acetaminophen challenge caused significant increases in the levels of bilirubin and liver enzymes (AST, ALT, ALP, and LDH), while TP and ALB levels were reduced significantly. Histopathologic assessments showed that severe glycogen storage in hepatocytes, hepatocellular degeneration and necrosis, mononuclear cell infiltration in portal area, dilation of central veins, and capillarization also reduced in KT/acetaminophen group compared to acetaminophen-treated mice. In conclusion, these findings suggest that KT has protective effect on acetaminophen-induced hepatotoxicity.

Hepatoprotective activity of punarnavashtak kwath, an Ayurvedic formulation, against CCl4-induced hepatotoxicity in rats and on the HepG2 cell line

Objective: Punarnavashtak kwath (PNK) is a classical Ayurvedic formulation, mentioned in Ayurvedic literature Bhaishajya Ratnavali, for hepatic disorders and asthma. This study investigated the hepatoprotective activity of PNK to validate the traditional use of this formulation.Materials and methods: PNK was prepared in the laboratory according to the method given in Ayurvedic literature. Phytochemical screening was performed to determine the presence of phytoconstituents. Hepatoprotective activity was evaluated against CCl4-induced hepatotoxicity in rats and by its effect on the HepG2 cell line.Results: Preliminary phytochemical screening revealed the presence of alkaloids, tannins, flavonoids, saponins, and a bitter principle in PNK. Administration of PNK produced significant hepatoprotective effect as demonstrated by decreased levels of serum liver marker enzymes such as aspartate transaminase, serum alanine transaminase, serum alkaline phosphatase, and serum bilirubin and an increase in protein level. Thiopentone-induced sleeping time was also decreased in the PNK-treated animals compared with the CCl4-treated group. It also showed antioxidant activity by increase in activity of glutathione, superoxide dismutase, and catalase and by a decrease in thiobarbituric acid reactive substance level compared with the CCl4-treated group. Results of a histopathological study also support the hepatoprotective activity of PNK. Investigation carried out on the HepG2 cell line depicted significant increase in viability of cells exposed to PNK as compared with CCl4-treated cells.Discussion and Conclusion: It can be concluded that PNK protects hepatocytes from CCl4-induced liver damages due to its antioxidant effect on hepatocytes. An in vitro study on HepG2 cell lines also supports its protective effect.

Antioxidant Potential of Momordica Charantia in Ammonium Chloride-Induced Hyperammonemic Rats.

The present study was aimed to investigate the antioxidant potential of Momordica charantia fruit extract (MCE) in ammonium chloride-induced (AC) hyperammonemic rats. Experimental hyperammonemia was induced in adult male Wistar rats (180–200 g) by intraperitoneal injections of ammonium chloride (100 mg kg−1 body weight) thrice a week. The effect of oral administration (thrice a week for 8 consecutive weeks) of MCE (300 mg kg−1 body weight) on blood ammonia, plasma urea, serum liver marker enzymes and oxidative stress biomarkers in normal and experimental animals was analyzed. Hyperammonemic rats showed a significant increase in the activities of thiobarbituric acid reactive substances, hydroperoxides and liver markers (alanine transaminase, aspartate transaminase and alkaline phosphatase), and the levels of glutathione peroxidase, superoxide dismutase, catalase and reduced glutathione were decreased in the liver and brain tissues. Treatment with MCE normalized the above-mentioned changes in hyperammonemic rats by reversing the oxidant-antioxidant imbalance during AC-induced hyperammonemia, and offered protection against hyperammonemia. Our results indicate that MCE exerting the antioxidant potentials and maintaining the cellular integrity of the liver tissue could offer protection against AC-induced hyperammonemia. However, the exact underlying mechanism is yet to be investigated, and examination of the efficacy of the active constituents of the M. charantia on hyperammonemia is desirable.

Effect of phenolic compounds released during degradation of Coir pith by &lt;i&gt;Oscillatoria annae&lt;/i&gt; on Albino rat (&lt;i&gt;Rattus norvegicus&lt;/i&gt;)

This study was carried out to investigate the effect of degraded coir pith based cyanobacterial culture filtrate on Rattus norvegicus. The culture filtrate containing phenolic compound was administered at a rateof 42 mg/Kg for 15 days and its effect on serum glucose, protein, creatinine, urea, uric acid, alkaline phosphate (ALP), serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT) and sperm analysis was studied. The results showed a significant reduction in the levels of serum glucose and liver marker enzymes while serum protein and renal function test showed normal level in both experimental and control rats. Also, a significant reduction in semen count was reported. The results suggested that the phenolic compoundof the culture filtrate appears to be non toxic in the tested animals

Pyridoxine mitigates cadmium induced hepatic cytotoxicity and oxidative stress

Therapeutic potential of pyridoxine (vit B6) was evaluated against cadmium induced hepatic cytotoxicity in culture and oxidative stress in rats. Nonmalignant “Chang” liver cell culture was exposed to Cd (cadmium chloride) that produced cytotoxicity in terms of increase in cell growth inhibition rate, alanine aminotransferase, lactate dehydrogenase and lipid peroxidation, which was significantly mitigated by pyridoxine in a concentration dependent manner. Acute exposure to Cd (6.5 mg/kg body weight; ip once only) produced a condition of hepatic oxidative stress by substantially increasing lipid peroxidation and oxidized glutathione level along with corresponding decrease in reduced glutathione and various antioxidant enzymes, i.e., superoxide dismutase, catalase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase. Cadmium administration significantly increased the leakage of liver marker enzymes in serum, i.e., transaminases, alkaline phosphatase and lactate dehydrogenase. Therapy with pyridoxine after 3 h of Cd administration decreased the release of serum transaminases, alkaline phosphatase and lactate dehydrogenase towards control. Administration of pyridoxine inhibited lipid peroxidation and formation of oxidized glutathione, increased the reduced glutathione level and restored the activities of aforesaid antioxidant enzymes towards control. The observations clearly demonstrated that pyridoxine treatment mitigates cadmium induced hepatic cytotoxicity and oxidative stress and provides evidence that it may be used clinically against Cd-induced hepatic toxicity.

Hepatic endogenous defense potential of propolis after mercury intoxication

Exposure to mercuric chloride (HgCl(2) ; 5 mg kg(-1) body weight; i.p.) induced oxidative stress in mice and substantially increased lipid peroxidation (LPO) and oxidized glutathione (GSSG) levels, decreased the level of reduced glutathione (GSH) and various antioxidant enzymes in liver and also increased the activities of liver marker enzymes in serum. Therapy with propolis extract, a resinous wax-like beehive product (200 mg kg(-1) orally, after mercury administration), for 3 days inhibited LPO and the formation of GSSG and increased the level of GSH in the liver. Release of serum transaminases, alkaline phosphatase, lactate dehydrogenase and γ-glutamyl transpeptidase were significantly restored after propolis treatment. The activities of antioxidant enzymes, that is, superoxide dismutase, catalase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase, were also concomitantly restored towards normal levels after propolis administration. These observations clearly demonstrate that propolis treatment augments antioxidant defense against mercury-induced toxicity and provide evidence that propolis has therapeutic potential as a hepatoprotective agent.

Hepatoprotective and Antioxidant Activities ofVernonia amygdalinaon Acetaminophen-Induced Hepatic Damage in Mice

Vernonia amygdalina Del. (Family Compositae) is used in Nigerian folk medicine as a tonic and remedy against constipation, fever, high blood pressure, and many infectious diseases. We have evaluated the hepatoprotective and antioxidant effects of an aqueous extract of V. amygdalina leaves against acetaminophen-induced hepatotoxicity and oxidative stress in mice in vivo. Activities of liver marker enzymes in serum (glutamate-oxaloacetate transaminase, glutamate-pyruvate transaminase, lactate dehydrogenase, and alkaline phosphatase) and bilirubin levels were determined colorimetrically, while catalase activity, lipid peroxidation products, thiobarbituric acid-reactive substances (TBARS), iron, and total protein concentrations were measured in liver homogenate. Acetaminophen challenge (300 mg/kg, i.p) for 7 days caused significant (P < .01) increases in the levels of bilirubin, liver enzymes, TBARS, and iron, while catalase activity and total protein level were reduced significantly (P < .01). Preadministration of V. amygdalina resulted in a dose-dependent (50-100 mg/kg) reversal of acetaminophen-induced alterations of all the liver function parameters by 51.9-84.9%. Suppression of acetaminophen-induced lipid peroxidation and oxidative stress by the extract was also dose-dependent (50-100 mg/kg). The results of this study suggest that V. amygdalina elicits hepatoprotectivity through antioxidant activity on acetaminophen-induced hepatic damage in mice.

Protein isolate from the herb, Phyllanthus niruri L. (Euphorbiaceae), plays hepatoprotective role against carbon tetrachloride induced liver damage via its antioxidant properties

Phyllanthus niruri L. (Euphorbiaceae) ( P. niruri) is a well-known hepatoprotective herbal plant. In the present study, hepatoprotective potential of the protein isolate of P. niruri was investigated against carbon tetrachloride (CCl 4) induced liver damage in vivo. Protein isolate of P. niruri was intraperitoneally injected in mice either prior to (preventive) or after the induction of toxicity (curative). Levels of different liver marker enzymes in serum and different anti-oxidant enzymes, as well as lipid peroxidation products and glutathione (GSH) in liver homogenates were measured in normal, control (toxicity induced) and protein isolate treated mice. Administration of CCl 4 increased the serum glutamate pyruvate transaminase (GPT) and alkaline phosphatase (ALP) levels of mice sera along with increased lipid peroxidation and reduced levels of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) in the liver. Treatment with the protein isolate of P. niruri significantly altered these changes to almost normal. The protein isolate also showed protective properties as was evidenced in histopathological studies. Results suggest that the protein isolate of P. niruri protects liver tissues against oxidative damage and somehow helps stimulating repair mechanism present in liver. It could be used as an effective hepatoprotector against CCl 4 induced liver damage.

The protein fraction of Phyllanthus niruri plays a protective role against acetaminophen induced hepatic disorder via its antioxidant properties

The aim of this study was to investigate the hepatoprotective action of the protein fraction of Phyllanthus niruri against acetaminophen (APAP) hepatotoxicity. The partially purified protein fraction of P. niruri was injected intraperitoneally in mice either prior to (preventive) or after the induction of toxicity (curative). Levels of different liver marker enzymes in serum and different antioxidant enzymes, as well as lipid peroxidation in total liver homogenates were measured in normal, control (toxicity induced) and P. niruri protein fraction-treated mice. P. niruri significantly reduced the elevated glutamate pyruvate transaminase (GPT) and alkaline phosphatase (ALP) levels in the sera of toxicity induced mice, compared with the control group. Lipid peroxidation levels were also reduced in mice treated with P. niruri protein fraction compared with the APAP treated control group. Among the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST) levels were restored to almost normal levels compared with the control group. P. niruri treatment also enhanced reduced hepatic glutathione (GSH) levels caused by APAP administration. The results demonstrated that the protein fraction of P. niruri protected liver tissues against oxidative stress in mice, probably acting by increasing antioxidative defense.