Rise In Serum Enzymes Research Articles

Hepatoprotective Activity of Ficus religiosa Leaf Extract in Rats

Ficus religiosa was investigated for its possible protective effect against paracetamol and CCl4-induced hepatic damage. IV administration of a sub-lethal dose of paracetamol (500 mg/kg) produced liver damage in rats as manifested by the rise in serum level of transaminases (AST and ALT). Ttreatment of rats with Ficus religiosa(200 mg/kg) prevented the paracetamol-induced rise in serum enzymes. The hepatotoxic dose of CCl4 (1.5 ml/kg; orally) also raised the serum AST and ALT levels. The same dose of Ficus religiosa(200 mg/kg) was able to prevent the CCl4-induced rise in serum enzymes. These results indicate that Ficus religiosa possesses hepatoprotective activity.

Hepatoprotective and antioxidant effects of fish oil on isoniazid-rifampin induced hepatotoxicity in rats

In the present study hepatoprotective and antioxidant potential of fish oil (cod liver oil) against isoniazid and rifampin combination (INH-RMP)-induced toxicity was evaluated in rats. Administration of (50mg INH+100mg RMP/kg/day, intraperitonially [i.p]) for 14 daysproducedliver injury that was evident from elevated levels of serum marker enzymes, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP), and histopathological changes. The drug treatment caused significant changes in the cellular redox status as reflected by about 75% decrease in the level of serum total antioxidant capacity (TAC), a marked decrease in reduced glutathione (GSH) level, an increased in lipid peroxidation (LPO) in the liver. Fish oil treatment (4ml/kg/day, i.p.) 5–6 hrprior to (INH-RMP) dose, markedlyprevented the rise in serum enzymes levelselicited by the drugs. The histopathological alterations were also improved. Remarkably, there was a complete reversal of the changes in the levels of GSH and LPO, and partial recovery of TAC in the animals receiving fish oil along with (INH-RMP). These observations support the mechanistic role of strong antioxidant property of fish oil in the protection of hepatic injury. This study suggests the importance of fish oil as a hepatoprotective and antioxidant dietary supplement, particularly in the patients receiving anti-tubercular therapy which are at a risk of hepatotoxicity.

The hepatoprotective effect of coumarin and coumarin derivates on carbon tetrachloride-induced hepatic injury by antioxidative activities in rats

Coumarins are a vast group of natural compounds and some of them possess antioxidant activities. The comparison of the antioxidant activity of some coumarins with various chemical molecular structure has not been investigated in previous studies. Therefore, this study was aimed to investigate the hepatoprotective effect against carbon tetrachloride (CCl(4)) -induced hepatic injury by coumarin (1,2-benzopyrone) and coumarin derivatives, esculetin (6,7-dihydroxycoumarin), scoparone (6,7-dimethoxycoumarin), and 4-methylumbelliferone (7-hyroxy-4-methyl) in male Sprague-Dawley rats. Product of lipid peroxidation, malondialdehyde (MDA), activities of antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) were evaluated for oxidative stress in hepatic injury. Gamma glutamyl transpeptidase (GGT), lactate dehydrogenase (LDH) were detected in plasma as a biomarker of hepatic injury. Significantly elevated levels of MDA and lowered levels of SOD and CAT activities were observed in liver of rats exposed to CCl(4), when compared to control values. Similarly, administration of CCl(4) increased LDH and GGT levels in serum. Pre-treatment of rats with esculetin (35mgkg(-1), orally) and scoparone (35mgkg(-1), orally) significantly prevented CCl(4)-induced decrease in MDA levels and increase in SOD and CAT, whereas 4-methylumbelliferone (35mgkg(-1)) and coumarin (30mgkg(-1)) had no effect against CCl(4)-induced rise in serum enzymes. Esculetin and scoparone also showed protective properties as was evidenced in reduced LDH and GGT levels in serum. The results of this study indicate that the chemical structures of coumarins play an important role in the prevention of oxidative stress.

Protective effects of coumarin and coumarin derivatives against carbon tetrachloride-induced acute hepatotoxicity in rats

The comparison of the antioxidant activity of some coumarins with their molecular structure is well determined. However, the protective function of coumarins with various chemical structures against liver toxicity has not yet been well established. Therefore, the aim of this study was to evaluate the possible cytoprotective properties of coumarin and some coumarin derivatives against CCl 4 (carbon tetrachloride)-induced hepatotoxicity. Coumarin (1,2-benzopyrone) and coumarin derivatives esculetin (6,7-dihydroxycoumarin), scoparone (6,7-dimethoxycoumarin) and 4-methylumbelliferone (7-hyroxy-4-methyl) were examined for their protective effect against CCl 4-induced hepatotoxicity in Male Sprague-Dawley rats. A single toxic dose of CCl 4 (1.25 ml kg −1, orally) produced liver damage in rats, seen histologically as centrilobular necrosis. Administration of CCl 4 increased serum enzyme levels of aspartate transaminase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP). Pre-treatment of rats with esculetin (31.15 mg kg −1, orally) and scoparone (35 mg kg −1, orally) significantly prevented CCl 4-induced increase in serum enzymes, whereas 4-methylumbelliferone (35 mg kg −1) and coumarin (30 mg kg −1) had no effect against CCl 4-induced rise in serum enzymes. Morphological findings were consistent with the plasma transaminase observations. Among the coumarin analogs, esculetin, which possesses orthodihydroxy coumarins, showed the strongest protective effect against CCl 4-induced liver damage, followed by scoparone, 4-methylumbelliferone and coumarin, respectively. The results of this study indicate that the chemical structures of coumarins play an important role in the prevention of liver toxicity.

Studies on the protective effects of caffeic acid and quercetin on chemical-induced hepatotoxicity in rodents

Caffeic acid and quercetin, the well-known phenolic compounds widely present in the plant kingdom, were investigated for their possible protective effects against paracetamol and CCl4-induced hepatic damage. Paracetamol at the oral dose of 1 g/kg produced 100% mortality in mice while pretreatment of separate groups of animals with caffeic acid (6 mg/kg) and quercetin (10 mg/kg) reduced the death rate to 20% and 30%, respectively. Oral administration of sub-lethal dose of paracetamol (640 mg/kg) produced liver damage in rats as manifested by the significant (P<0.01) rise in serum levels of aminotransferases (aspartate transaminase (AST) and alanine transaminase (ALT)) compared to respective control values. The serum enzyme values were significantly (P<0.01) lowered on pretreatment of rats with either caffeic acid (6 mg/kg) or quercetin (10 mg/kg). Similarly, the hepatotoxic dose of CCl4 (1.5 ml/kg; orally) also raised significantly (P<0.05) the serum AST and ALT levels as compared to control values. The same dose of the caffeic acid and quercetin was able to prevent CCl4-induced rise in serum enzymes. Caffeic acid and quercetin also prevented the CCl4-induced prolongation in pentobarbital sleeping time confirming their hepatoprotectivity. These results indicate that caffeic acid and quercetin exhibited hepatoprotective activity possibly through multiple mechanisms.

Protective effect of rutin on paracetamol- and CCl 4-induced hepatotoxicity in rodents

Rutin, a well-known flavonoid was investigated for its possible protective effect against paracetamol- and CCl 4-induced hepatic damage. Paracetamol produced 100% mortality at the dose of 1 g/kg in mice while pre-treatment of animals with rutin (20 mg/kg) reduced the death rate to 40%. Oral administration of a sub-lethal dose of paracetamol (640 mg/kg) produced liver damage in rats as manifested by the rise in serum level of transaminases (AST and ALT). Pre-treatment of rats with rutin (20 mg/kg) prevented the paracetamol-induced rise in serum enzymes. The hepatotoxic dose of CCl 4 (1.5 ml/kg; orally) also raised the serum AST and ALT levels. The same dose of rutin (20 mg/kg) was able to prevent the CCl 4-induced rise in serum enzymes. Rutin also prevented the CCl 4-induced prolongation in pentobarbital sleeping time confirming its hepatoprotectivity. These results indicate that rutin possesses hepatoprotective activity and the presence of this compound in Artemisia scoparia may explain the folkloric use of the plant in liver damage.

Hypoglycemic and hypolipidemic effects of diacetodibutyl disulphide

The hyperlipidemia, fatty liver and the high levels of liver and kidney thiobarbituric acid reactive substances (TBARS) observed in rats which were fed ethanol for 45 days, could be significantly reduced by feeding diacetodibutyl disulphide (DADBDS). Ethanol-induced hypoproteinemia and the rise in serum enzymes like AST (EC 2.6.1.10), ALT (EC 2.6.1.2) and ALP (EC 3.1.3.1) could also be ameliorated by DADBDS. Feeding of this compound to normal rats did not produce any change in serum or tissue lipid levels or serum enzymes or tissue TBARS except a moderate reduction in serum triacyl glycerols. DADBDS feeding to rats maintained on a high lipid diet could also reduce the serum and tissue lipid levels and also reduce the serum transaminases.DADBDS which is an aliphatic disulphide could produce hypolipidemic effects in rats fed a single large dose of ethanol, whereas dimenthol disulphide which is an aromatic disulphide was not useful as a hypolipidemic agent. Perhaps hypolipidemic effects are shown only by aliphatic disulphides and not by aromatic disulphides. Feeding of 100 mg DADBDS per kg body weight to normal fasted rats produced a mild hypoglycemia, but higher doses produced a hyperglycemic effect. This dose of DADBDS increased the serum insulin levels and reduced blood glucose levels in fasted diabetic rats, but DADBDS feeding did not alter the serum insulin levels in fasted normal rats. DADBDS is odourless and tasteless in 1% solution and it could be a better substitute for garlic for hypoglycemic and hypolipidemic studies.

AN ASSESSMENT OF THE POTENTIAL OF PROTOPINE TO INHIBIT MICROSOMAL DRUG METABOLISING ENZYMES AND PREVENT CHEMICAL-INDUCED HEPATOTOXICITY IN RODENTS

The potential of protopine to inhibit microsomal drug metabolising enzymes (MDM E) and prevent paracetamol- and CCl4-induced hepatotoxicity was studied in rats. Paracetamol at the dose of 640 mg kg−1produced hepatic damage in rats as manifested by the rise in serum levels of aspartate transaminase (AST) and alanine transaminase (ALT) to 972±186 and 624±131 IU (mean±sem;n=10), respectively, compared to respective control values of 101±29 and 64±18 IU. Pretreatment of rats with protopine (11 mg kg−1, orally twice daily for 2 days) lowered significantly the respective serum AST and ALT levels (P<0.05) to 289±52 and 178±43 IU. The hepatotoxic dose of CCl4(1.5 ml kg−1; orally) raised serum AST and ALT levels to 543±89 and 387±69 IU (mean±sem;n=10), respectively, compared to respective control values of 98±28 and 56±17 IU. The same dose of protopine (11 mg kg−1) was able to prevent significantly (P<0.05), the CCl4-induced rise in serum enzymes and the estimated values of AST and ALT were 168±36 and 93±28 IU, respectively. Protopine caused prolongation (P<0.05) in pentobarbital (55 mg kg−1)-induced sleep as well as potentiated strychnine-induced toxicity in rats, suggestive of an inhibitory effect on MDME. These results indicate that protopine exhibits anti-hepatotoxic action which may be mediated through inhibition of MDME.

ESCULETIN PREVENTS LIVER DAMAGE INDUCED BY PARACETAMOL AND CCL4

Esculetin, a phenolic compound found inCichorium intybusandBougainvllra spectabilliswas investigated for its possible protective effect against paracetamol and CCl4-induced hepatic damage. Paracetamol produced 100% mortality at the dose of 1 g kg−1in mice while pre-treatment of animals with esculetin (6 mg kg−1) reduced the death rate to 40%. Oral administration of paracetamol (640 mg kg−1) produced liver damage in rats as manifested by the rise in serum enzyme levels of alkaline phosphatase (ALP) and aminotransferases (AST and ALT). Pre-treatment of rats with esculetin (6 mg kg−1) prevented the paracetamol-induced rise in serum enzymes. The hepatotoxic dose of CCl4(1.5 ml kg−1; orally) also raised serum ALP, AST and ALT levels. The same dose of esculetin (6 mg kg−1) was able to prevent the CCl4-induced rise in serum enzymes. Esculetin also prevented CCl4-induced prolongation in pentobarbital sleeping time confirming hepatoprotectivity. These results indicate that esculetin possesses anti-hepatotoxic activity and the presence of this compound inCichorium intybusandBougainvllra spectabillismay explain the folkloric use of these plants in liver damage.

Effect of Rubia cordifolia extract on acetaminophen and CCl4‐induced hepatotoxicity

AbstractThe hepatoprotective activity of an aqueous‐methanol extract of Rubia cordifolia (Rubiaceae) was investigated against acetaminophen and CCl4‐induced hepatic damage. Acetaminophen produced 100% mortality at a dose of 1 g/kg in mice while pretreatment of animals with plant extract (500 mg/kg) reduced the death rate to 30%. Acetaminophen at a dose of 640 mg/kg produced liver damage in rats as manifested by the rise in serum levels of GOT and GPT to 1447±182 and 899±201 IU/L (n = 10) respectively, compared with respective control values of 97±10 and 36±11. Pretreatment of rats with plant extract (500 mg/kg) lowered significantly (p &lt;0.005) the respective serum GOT and GPT levels to 161±48 and 73±29. Similarly, hepatotoxic dose of CCl4 (1.5 mL/kg; orally) raised the serum transaminases (GOT and GPT) levels to 422±102 and 354±74 IU/L (n = 10) respectively compared with respective control values of 99±15 and 29±08 IU/L. The same dose of plant extract (500 mg/kg) was able to prevent significantly (p &lt;0.01) the CCl4‐induced rise in serum enzymes and the estimated values of GOT and GPT were 95±09 and 33±07 IU/L, respectively. Moreover, it prevented CCl4‐induced prolongation in pentobarbital sleeping time confirming the hepatoprotective effects of the extract.

Studies on protective effect of Cyperus Scariosus extract on acetaminophen and CCl 4-induced hepatotoxicity

1. 1. The hepatoprotective activity of aqueous-methanolic extract of Cyperus scariosus (Cyperaceae) was investigated against acetaminophen and CCl 4-induced hepatic damage. 2. 2. Acetaminophen produced 100% mortality at a dose of 1 g/kg in mice while pretreatment of animals with plant extract (500 mg/kg) reduced the death rate to 30%. 3. 3. Acetaminophen at a dose of 640 mg/kg produced liver damage in rats as manifested by the rise in serum levels of alkaline phosphatase (ALP), glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT) to 430 ± 68, 867 ± 305 and 732 ± 212 IU/1 ( n = 10) respectively, compared to respective control values of 202 ± 36, 59 ± 14 and 38 ± 7. 4. 4. Pretreatment of rats with plant extract (500 mg/kg) significantly lowered ( P < 0.05) the respective serum ALP, GOT and GPT levels to 192 ± 31, 63 ± 9 and 35 ± 8. 5. 5. The hepatotoxic dose of CCl 4 (1.5ml/kg; orally) raised serum ALP, GOT and GPT levels to 328 ± 30, 493 ± 102 and 357 ± 109 IU/1 ( n = 10) respectively, compared to respective control values of 177 ± 21, 106 ± 15 and 47 ± 12. 6. 6. The same dose of plant extract (500 mg/kg) was able to significantly prevent ( P < 0.05) CCl 4-induced rise in serum enzymes and the estimated values of ALP, GOT and GPT were 220 ± 30, 207 ± 95 and 75 ± 38, respectively. 7. 7. The plant extract also prevented CCl 4-induced prolongation in pentobarbital sleeping time confirming hepatoprotectivity. 8. 8. These results indicate that the Cyperus scariosus possesses hepatoprotective activity and thus, rationalizes the folkloric use of this plant in hepato-biliary disorders.

Evaluation of the liver protective potential of Cichorium intybus seed extract on Acetaminophen and CCl 4-induced damage

The hepatoprotective activity of aqueous-methanolic extract of Cichorium intybus seeds was investigated against acetaminophen and CCl(4)-induced hepatic damage. Acetaminophen produced 100% mortality at the dose of 1 g/kg in mice while pretreatment of animals with plant extract (500mg/kg) reduced the death rate to 30%. Acetaminophen at the dose of 640 mg/kg produced liver damage in rats as manifested by the significant (P < 0.01) rise in serum levels of alkaline phosphatase (ALP), GOT and GPT to 393 ± 28, 767 ± 215 and 692 ± 191 IU/L (n = 10) respectively, compared to respective control values of 198 ± 15, 76 ± 07 and 39 ± 09. Pretreatment of rats with plant extract (500 mg/kg) significantly lowered (P < 0.01), the respective serum ALP, GOT and GPT levels to 228 ± 16, 68 ± 10 and 41 ± 08. Similarly, a hepatotoxic dose of CCl(4) (1.5 mL/kg; orally) significantly raised (P < 0.01), the serum ALP, GOT and GPT levels to 312 ± 20, 503 ± 98 and 407 ± 109 IU/L (n = 10) respectively, compared to respective control values of 215 ± 16, 79 ± 18 and 49 ± 10. The same dose of plant extract (500 mg/kg) was able to prevent significantly (P < 0.05) the CCl(4)-induced rise in serum enzymes and the estimated values of ALP, GOT and GPT were 222 ± 27, 114 ± 23 and 68 ± 14 respectively. Moreover, it prevented CCl(4)-induced prolongation in pentobarbital sleeping time confirming hepatoprotectivity and validates the folkloric uses of this plant in liver damage.

Pericarditis after acute myocardial infarction.

Fifty-two (6.8%) of 779 patients admitted to a coronary monitoring unit with acute myocardial infarction developed a pericardial friction rub. A diagnosis of postmyocardial infarction syndrome was made in three of these.The course of the 52 patients with pericarditis was compared with that of a consecutive series of 100 patients without pericarditis. As a group those with pericarditis manifested a longer period of pyrexia, a greater rise in serum enzymes, and a higher incidence of major arrhythmias and of radiological pulmonary oedema. The Peel prognostic index, however, did not differ significantly in the two groups. The hospital mortality of the pericarditis group was not significantly different from that of the 727 non-pericarditis patients. No specially adverse features were found in a follow-up of the pericarditis group.Though the presence of a pericardial rub in the first few days after a myocardial infarction may be a sign of extensive myocardial damage and is associated with a relatively high incidence of ventricular fibrillation, it does not appear to influence the hospital mortality of patients treated in a monitoring unit.

Hypothermic peritoneal dialysis in the treatment of acute experimental hemorrhagic pancreatitis

Acute hemorrhagic pancreatitis was induced in dogs using a modification of the method of Elliot. Ten dogs received no therapy and eight died. Of nine dogs receiving intravenous Ringer's lactate solution, seven died. Hypothermic peritoneal dialysis was carried out in ten dogs, two of which died. The following observations were noted: 1. 1. Intravenous Ringer's lactate solution had no effect on the course of pancreatitis. 2. 2. The rise in serum enzymes was less in the hypothermic group. 3. 3. Hypothermic peritoneal dialysis markedly decreased the amount of hemorrhage and necrosis within the pancreas and the extent of generalized fat necrosis.

SERUM ENZYMES AND LACTIC DEHYDROGENASE ISOENZYMES AFTER EXERCISE AND TRAINING IN RATS.

After 16 hr exercise, untrained rats, in contrast to exercise-trained rats, show a marked rise in serum lactic dehydrogenase, aldolase, glutamic oxalacetic transaminase, glutamic pyruvic transaminase, and urea nitrogen. Electrophoretic studies reveal abnormal serum isoenzyme patterns indicating that excess lactic dehydrogenase is derived not only from muscle, but also from heart and probably other organs. Histopathologic studies and serum transaminase ratios support this conclusion. These findings are correlated with necrosis in muscle fibers and fatty changes in muscle, heart, and other organs of untrained rats after prolonged exercise and the absence of such changes in similarly exercise-trained animals. Alterations in cellular permeability best explain the rise in serum enzymes. However, exercise training does not prevent pathologic and serum enzyme and isoenzyme changes induced by epinephrine in oil. Moreover, the adrenergic blocking agent, Dibenamine, which ameliorates such changes induced by epinephrine or hypoxia, does not mitigate the effects of prolonged exercise in untrained rats. These findings suggest that the permeability changes induced by prolonged exercise are not due merely to the effects of hypoxia or of catecholamines released from the adrenal medulla, but are different and perhaps specific.

Serum enzyme and histopathologic changes in rats after cold exposure.

SummaryExposure of 2 groups of dry rats 16 hours to 1.7 and −5°C and a third group of wet rats 5 hours to 1.7°C on 2 successive days significantly increased levels of serum glutamic oxalacetic transaminase, serum aldolase and blood urea nitrogen. The blood urea nitrogen in all 3 groups and serum enzyme values in the 1st group were normal in 24 hours. The serum enzyme values in the 2nd and 3rd groups were normal in 3 and 6 days respectively. Mean body temperatures in the 3 groups at the end of the cold exposures were 38.2, 36.7 and 33°C respectively. The transient rise in serum enzymes coincided with a transient decrease in mean hematocrit and in glycogen in liver and muscle and lipid in the adrenal cortex, and leukocytosis. Many rats also showed transient fatty changes in the liver and, less frequently, in the kidney and heart