Antioxidant activity and protective effect of Turnera ulmifolia Linn. var. elegans against carbon tetrachloride-induced oxidative damage in rats

The present study aimed to determine whether the leaves of Turnera ulmifolia Linn. var. elegans extract exert significant antioxidant activity. The antioxidant activity of its hydroethanolic extract (HEETU) was evaluated by assessing (a) its radical scavenging ability in vitro, and (b) its in vivo effect on lipid peroxidation and antioxidant enzyme activities. The in vitro antioxidant assay (DPPH) clearly supported HEETU free radical scavenging potential. Moreover, glutathione content and antioxidant enzyme activities (glutathione peroxidase, superoxide dismutase and catalase) were significantly enhanced in CCl₄-treated rats due to oral HEETU-treatment (500 mg/kg b.w.) over 7 and 21 days. In addition, an improvement was observed in lipid peroxidation and serum biochemical parameters (aspartate aminotransferase and alanine aminotransferase), indicating a protective effect against CCl₄-induced liver injuries, confirmed by histopathological studies. The HEETU effect was comparable to the standard drug Legalon® (50 mg/kg b.w.) under the same experimental condition. Quantitative analysis of the HPLC extract revealed the presence of flavonoids, wich mediate the effects of antioxidant and oxidative stress. In conclusion, extract components exhibit antioxidant and hepatoprotective activities in vitro and in vivo.     

Acute paracetamol intoxication of starved mice leads to lipid peroxidation in vivo.

Lipid peroxidation was monitored in female mice in vivo by the measurement of exhalated hydrocarbons. In liver homogenates in vitro lipid peroxidation as determined by malondialdehyde formation, and hepatic total glutathione levels were measured. After a dose of 500 mg/kg i.p. of paracetamol, the hepatic glutathione of fed mice decreased from 61 nmoles/mg liver protein to 30 nmoles/mg, while the animals expired 5 nmoles of ethane/kga · hr. The same dose in starved mice led to a glutathione level of 6 nmoles/mg and an exhalation rate of 125–150 nmoles ethane/kg · hr. In vivo determined and post-mortem in vitro determined lipid peroxidation correlated with a coefficient of 0.66. If hepatic glutathione was depleted to the same extent by administration of diethylmaleate, no significant lipid peroxidation was found. Our findings demonstrate that the drug-induced depletion of liver glutathione leads in vivo to lipid peroxidation, provided that the glutathione level has been diminished by starvation. The data indicate that glutathione depletion alone by other mechanisms does not account for lipid peroxidation. Hence the hepatoprotective role of liver glutathione against drug-induced liver injury has to be reconsidered in detail. This investigation shows a suitable model for such studies.     

Biochemical aspects of the protective action of propyl gallate on liver injury in rats poisoned with carbon tetrachloride.

Liver injury in rats intoxicated with a high dose of CCl₄ (2.5 ml/kg, po) is partially prevented by propyl gallate. The accumulation of hepatic triglycerides and the release of liver enzymes into the plasma are more effectively inhibited by this antioxidant in rats given a smaller dose of the hepatotoxin (0.25 ml/kg, po). The antioxidant activity of propyl gallate, administered in vivo, estimated by means of the production of malonyl dialdehyde in liver homogenates in vitro, has been found to decrease progressively after treatment. The concentration of nonesterified fatty acids in the serum is not affected by dosing with propyl gallate. However, propyl gallate releases the block in triglyceride secretion from the liver that occurs after administration of CCl₄. Furthermore, both the uptake of CCl₄ by the liver and the early steps of the free radical reaction (incorporation of labeled metabolites of ¹⁴CCl₄ and double bond shifting in microsomal unsaturated lipids) are unchanged by concomitant dosing with propyl gallate. This free radical scavenger, when administered in discrete doses, more markedly influences both CCl₄ liver damage and the efficiency of the hepatic drug metabolizing enzyme system. This effect in vivo is consistent with the reported in vitro interaction of propyl gallate with microsomal electron transport. These findings indicate that propyl gallate partially interferes with the enzymes bound to the endoplasmic reticulum, but affects the secondary phenomena of lipid peroxidation at the level where lipoproteins are secreted and/or the permeability of plasma membrane is altered.     

The effects of adriamycin in vitro and in vivo on hepatic microsomal drug-metabolizing enzymes: role of microsomal lipid peroxidation

The quinone-containing anticancer drug adriamycin augments the reduction of dioxygen to reactive oxygen species and thereby stimulates (sixfold) NADPH-dependent microsomal lipid peroxidation. In vitro the extensive adriamycin-promoted peroxidation depleted (85%) rat liver microsomal cytochrome P-450, severely inhibited cytochrome P-450-dependent monooxygenation (70%), and glucose-6-phosphatase activity (80%), and activated (450%) UDP-glucuronyltransferase activity. When lipid peroxidation was blocked by EDTA, adriamycin selectively decreased cytochrome P-450 and aminopyrine N-demethylase activity; NADPH-cytochrome c reductase, UDP-glucuronyltransferase, and glucose-6-phosphatase activities were unchanged. Washing and resedimenting peroxidized microsomes to remove adriamycin and soluble lipid peroxidation products failed to restore enzyme activities to control values. Adriamycin administered subacutely (5 mg/kg × three doses) to rats significantly descreased hepatic microsomal cytochrome P-450 content and reduced aminopyrine N-demethylase and NADPH-cytochrome c reductase activities compared to saline-treated controls. Microsomal lipid peroxidation was increased following the above adriamycin treatment. Thus, these data suggested that adriamycin was capable of impairing hepatic drug metabolism in vitro by stimulating membrane lipid peroxidation in a manner similar to carbon tetrachloride; the mechanism by which adriamycin treatment in vivo decreased the activity of the drug monooxygenase system remains unclear.     

Hepatoprotective and Antioxidant Activity of Dunaliella salina in Paracetamol-induced Acute Toxicity in Rats

Paracetamol has a reasonable safety profile when taken in therapeutic doses. However, it could induce hepatotoxicity and even more severe fatal acute hepatic damage when taken in an overdose. The green alga, Dunaliella salina was investigated for hepatoprotective and antioxidant activity against paracetamol-induced liver damage in rats. Male albino Wistar rats overdosed with paracetamol showed liver damage and oxidative stress as indicated by significantly (P<0.05) increased serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total and direct bilirubin, malondialdehyde, cholesterol and nitric oxide. At the same time, there were decreased activities of serum superoxide dismutase and total antioxidant capacity compared with the control group. Treatment with D. salina methanol extract at doses of 500 and 1000 mg/kg body weight or silymarin could significantly (P<0.05) decrease the liver damage marker enzymes, total and direct bilirubin, malondialdehyde, cholesterol and nitric oxide levels and increase the activities of superoxide dismutase and total antioxidant capacity in serum when compared with paracetamol intoxicated group. Liver histopathology also showed that D. salina reduced the centrilobular necrosis, congestion and inflammatory cell infiltration evoked by paracetamol overdose. These results suggest that D. salina exhibits a potent hepatoprotective effect on paracetamol-induced liver damage in rats, which may be due to both the increase of antioxidant enzymes activity and inhibition of lipid peroxidation.     

Preliminary characterization,antioxidant activity in vitro and hepatoprotective effect on acute alcohol-induced liver injury in mice of polysaccharides from the peduncles of Hovenia dulcis

The fresh fleshy peduncles of Hovenia dulcis have been used as a food supplement and traditional herbal medicine for the treatment of liver diseases and alcoholic poisoning for more than a millennium. The objectives of the present study, therefore, were to determine the antioxidant activity of polysaccharides from the peduncles of H. dulcis (HDPS) and to evaluate its hepatoprotective effect on acute alcohol-induced liver injury in mice. HDPS, prepared by hot water extraction, ethanol precipitation and treatment of macroporous resin, was found to be non-starch polysaccharide and mainly composed of galactose, arabinose, rhamnose and galacturonic acid. In in vitro antioxidant assay, HDPS exhibited high superoxide radical scavenging activity, strong inhibition effect on lipid peroxidation and a medium ferrous ion-chelating activity. For hepatoprotective activity in vivo, the administration of HDPS significantly decreased the serum levels of alanine aminotransferase and aspartate aminotransferase, significantly decreased the liver level of malondialdehyde and remarkably restored the liver activities of superoxide dismutase and glutathione peroxidase in alcohol-induced liver injury mice. The results suggested that HDPS had a significant protective effect against acute alcohol-induced liver injury possibly via its antioxidant activity to protect biological systems against the oxidative stress.     

Effect of a human pharmaceutical carbamazepine on antioxidant responses in brain of a model teleost in vitro: an efficient approach to biomonitoring

Residual pharmaceuticals are generally recognized as relevant sources of aquatic environmental pollutants. In this study, the effects of carbamazepine (CBZ) on the antioxidant defense system in the brain of rainbow trout in vitro were studied. The brain homogenates were incubated with various concentrations of CBZ (1.0 µg l^?1, 0.2 mg l^?1 or 2.0 mg l^?1) for 0, 60, 120 min. After incubation, oxidative stress indices (lipid peroxidation and carbonyl protein), antioxidant enzymes (superoxide dismutase, glutathione reductase and glutathione peroxidase) and nonenzymatic antioxidant (reduced glutathione) in each samples were measured. Based on the results, the brain homogenates performed adaptive responses to CBZ‐induced stress at environmental concentration (1.0 µg l^?1). With increased CBZ concentrations (0.2 or 2.0 mg l^?1), oxidative stress was apparent as reflected by the significant higher levels of oxidative indices, together with the significant inhibition of all antioxidant enzymes activities and reduced glutathione content. Compared with previous studies in vivo, the brain homogenates showed more sensitive antioxidant responses to CBZ stress. In conclusion, the brain homogenates of rainbow trout could be used as an efficient model system in aquatic risk assessment, but more detailed laboratory studies are needed before these findings could be established as special biomarkers for monitoring residual pharmaceuticals in aquatic environment. Copyright © 2010 John Wiley & Sons, Ltd.     

A mechanism of paraquat toxicity in mice and rats.

The purpose of this study was to investigate the hypothesis that paraquat toxicity results from cyclic reduction-oxidation of paraquat in vivo, with subsequent generation of superoxide radicals and initiation of lipid peroxidation. Phenobarbital pretreatment (0.1% in drinking water for 10 days) significantly increased the paraquat LD50 in mice, but only when the mice were continued on phenobarbital after paraquat administration. Phenobarbital, through its own metabolism, may be competing for electrons which might otherwise be utilized in paraquat reduction and thus decrease paraquat toxicity. Paraquat, given at 30 mg/kg ip to mice, significantly decreased liver concentrations of the water-soluble antioxidant, reduced glutathione, and lung concentrations of lipid-soluble antioxidants. The decrease in tissue antioxidants may reflect the initiation of lipid peroxidation by paraquat. Oxygen-tolerant rats (exposure to 85% oxygen for 7 days) have increased activities of pulmonary enzymes which combat lipid peroxidation. The paraquat Lt50 (median time to death) after 45 mg/kg of paraquat ip was significantly increased in oxygentolerant rats compared to room-air-exposed controls. Rats exposed to 100 ppm paraquat in the drinking water for 3 weeks had significantly elevated activities of lung glucose-6-phosphate dehydrogenase and glutathione reductase. The cross-tolerance of oxygen and paraquat and the induction by paraquat of pulmonary enzymes that supply reducing equivalents to combat oxidative damage support the proposal that paraquat may initiate lipid peroxidation in vivo.     

Protective effect of quercetin in gentamicin-induced oxidative stress in vitro and in vivo in blood cells. Effect on gentamicin antimicrobial activity

We have evaluated the effect of gentamicin and gentamicin plus quercetin on ROS production, endogenous antioxidant defenses (SOD and CAT) and lipid peroxidation in vitro on human leukocytes and in vivo on whole rat blood. Gentamicin generated ROS production in human leukocytes, produced a dual effect on both enzymes dosage-dependent and generated an increase in lipid peroxidation. Quercetin, in leukocytes stimulated by gentamicin, showed more inhibitory capacity in ROS production than the reference inhibitor (vitamin C) in mononuclear cells and a similar protective behavior at this inhibitor in polymorphonuclear cells. Quercetin, in both cellular systems, tend to level SOD and CAT activities, reaching basal values and could prevent lipidic peroxidation induced by gentamicin. The results in Wistar rats confirmed that therapeutic doses of gentamicin can induce oxidative stress in whole blood and that the gentamicin treatment plus quercetin can suppress ROS generation, collaborate with SOD and CAT and diminish lipid peroxidation. Finally, flavonoid and antibiotic association was evaluated on the antimicrobial activity in S. aureus and E. coli, showing that changes were not generated in the antibacterial activity of gentamicin against E. coli strains, while for strains of S. aureus a beneficial effect observes. Therefore, we have demonstrated that gentamicin could induce oxidative stress in human leukocytes and in whole blood of Wistar rats at therapeutic doses and that quercetin may to produce a protective effect on this oxidative stress generated without substantially modifying the antibacterial activity of gentamicin against E. coli strains, and it contributes to this activity against S. aureus strains.     

In Vivo and In Vitro Sevoflurane-Induced Lipid Peroxidation in Guinea-pig Liver Microsomes

Abstract: Sevoflurane is a recently introduced volatile inhalation anaesthetic and is already used commonly in Japan. We investigated the potential of sevoflurane to cause lipid peroxidation in vivo and in vitro. For the in vitro study, pentane formation in a mixture of guinea pig liver microsomes and sevoflurane in the presence of nicotinamide adenine dinucleotide phosphate (NADPH) was analyzed by gas chromatography. Under anaerobic conditions, pentane formed without sevoflurane, but sevoflurane potentiated this anaerobic pentane formation. Two antioxidant agents, vitamine E and glutathione, reduced the pentane formation induced by sevoflurane. In the in vivo study, 18 guinea pigs were exposed to air (control), 0.5% halothane, or 1.2% sevoflurane. The extent of lipid peroxidation and liver damage was investigated by measuring the level of thiobarbituric acid reactive products and serum transaminase (alanine-aminotransferase: ALAT and aspartate-aminotransferase: ASAT) activity 12 hr after exposure. Both halothane and sevoflurane significantly increased thiobarbituric acid-reactive products. The increase in thiobarbituric acid-reactive products seen with sevoflurane administration was half that seen with halothane. Sevoflurane increased the ALAT activity to the same extent as did halothane but did not increase the ASAT activity. We conclude that sevoflurane potentiates lipid peroxidation in guinea pig liver microsomes in vivo and in vitro. However, because the degree of liver damage as measured by transaminase activity was minimal and the mechanism of sevoflurane-induced lipid peroxidation is still unknown, we must be cautious in applying these results to humans.     

Cissus quadrangularis stem alleviates insulin resistance,oxidative injury and fatty liver disease in rats fed high fat plus fructose diet

The study evaluated the protective effects of Cissus quadrangularis stem extract (CQEt) on oxidant–antioxidant balance and insulin resistance (IR) in rats fed high fat–high fructose diet (HFFD) and also tested its free-radical scavenging property in vitro. Rats were fed either control diet or HFFD for 15 days, following which the diet was fortified with CQEt at a dose of 10 g/100 g diet. After 60 days, HFFD caused deleterious metabolic effects, including hyperglycemia, IR and liver dysfunction. Rats fed HFFD alone showed increased activities of hepatocellular enzymes in plasma, lipid deposition, significant decline in antioxidants, and elevated lipid peroxidation indices and protein carbonyl in liver. CQEt addition significantly improved insulin sensitivity, reduced liver damage and oxidative changes, and brought back the antioxidants and lipids towards normal. Histopathology of the liver confirmed the changes induced by HFFD and the heptoprotective effect of CQEt. The effects of CQEt in vivo were comparable with that of standard drug, metformin. Through in vitro assays, CQEt was found to contain large quantities of polyphenols, vitamins C and E. CQEt exhibited radical scavenging ability in a dose-dependent manner. These data suggest that CQEt affords hepatoprotection by its antioxidant and insulin-sensitizing activities.     

Anti-inflammatory and antioxidant potential of alginic acid isolated from the marine algae, Sargassum wightii on adjuvant-induced arthritic rats

The present study evaluated the anti-inflammatory and antioxidant potential of alginic acid isolated from brown algae Sargassum wightii in arthritic rats. Arthritis was induced in male Sprague–Dawley rats by intradermal injection of complete Freund’s adjuvant into the right hind paw, produce inflammation of the joint tissue. Paw edema volume, enzymes linked to inflammation such as cyclooxygenase, lipoxygenase and myeloperoxidase, and the level of ceruloplasmin, C-reactive protein and rheumatoid factor were evaluated in all the experimental groups. Oxidative stress during inflammation was analyzed by estimating lipid peroxidation and the activities of antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and non-enzymatic antioxidant, reduced glutathione. Alginic acid treatment (100 mg/kg) in arthritic rats exhibited reduced paw edema volume along with reduced activities of enzymes such as cyclooxygenase, lipoxygenase and myeloperoxidase. Reduction in the level of C-reactive protein, ceruloplasmin and rheumatoid factor were also observed in arthritic rats treated with alginic acid along with reduced lipid peroxidation and enhanced activities of antioxidant enzymes, which suggest the antioxidant potential of the compound. Histopathological analysis of paw tissue showed that alginic acid treatment reduced paw edema and inflammatory infiltration in arthritic rats. Overall results suggest that alginic acid isolated from Sargassum wightii exhibits potent anti-inflammatory and antioxidant activity, and can develop this marine alga as an alternative source for therapy and can be used as a drug candidate for the development of anti-inflammatory agent.     

Effect of Aerva lanata against hepatotoxicity of carbon tetrachloride in rats

The partially purified petroleum ether extractable fraction of the whole plant Aerva lanata (PF) was evaluated for the protective effect against liver damage induced by carbon tetra chloride (CCl₄) in Sprague Dawley rats. Rats were orally administered with PF (50 and 100 mg/kg body weight) for 14 days before CCl₄ challenge and 100 mg of PF alone for toxicity analysis without CCl₄ administration. The results showed that CCl₄ administration significantly damaged the liver as evident from histopathology and very high activity of serum and liver marker enzymes. It also reduced the antioxidant enzyme status of the animals. PF administration significantly reversed the histopathological changes and restored the elevated activities of liver marker enzymes and also enhanced the antioxidant enzyme activities. The extract also reduced hepatic lipid peroxidation and increased the serum total protein and albumin/globulin (A/G) ratio. Preliminary phytochemical analysis of PF showed the presence of alkaloids. These observations clearly indicate that PF contains antioxidant alkaloids capable of ameliorating the CCl₄-induced hepatic injury by virtue of its antioxidant activity.     

Lipid peroxidation and paraquat toxicity.

Paraquat, added in vitro, stimulated lipid peroxidation in lung microsomes obtained from mouse lung but not from rat lung. Pretreatment of mice with N, N'-diphenyl-p-phenylene diamine, an antioxidant, or a high carbohydrate diet prevented the stimulatory effects of paraquat on lipid peroxidation but did not protect the animals against the lethal effects of paraquat. Conjugated dienes were not elevated in vivo after a dose of paraquat in mice equivalent to twice the ld₅₀. Plasma and lung concentrations and edematogenic activities of paraquat and diquat were measured in rats after subcutaneous injections of these chemicals. At equimolar doses, diquat was less edematogenic and found at lower concentrations in lung than was paraquat, but, considering the greater efficacy of diquat in stimulating lipid peroxidation in vitro (R. Talcott, H. Shu and E. Wei, [24], these results indicate that the effects of bipyridinium herbicides in vitro may not be related to their mechanisms of toxicity in vivo.     

Effect of 4-methylpyrazole on antioxidant enzyme status and lipid peroxidation in the liver of rats after exposure to ethylene glycol and ethyl alcohol

BackgroundThe aim of the conducted studies was to evaluate the effect of 4-methylpyrazole, increasingly used in detoxifying treatments after ethylene glycol poisoning, on the activity of some antioxidant enzymes and lipid peroxidation formation in the liver of rats after experimental co-exposure to ethylene glycol and ethyl alcohol.MethodsThe trials were conducted on adult male Wistar rats. Ethylene glycol (EG) at the dose of 3.83 g/kg bw and ethyl alcohol (EA) at the dose of 1 g/kg bw were administered po, and 4-methylpyrazole (4-MP) at the dose of 0.01 g/kg bw was administered ip. Parameters of antioxidant balance were evaluated in hepatic cytosol, including the activity of the following enzymes: glutathione S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPx) and lipid peroxidation level (TBARS).ResultsThe results suggest that evaluation of the effects of administrated 4-MP after co-exposure to EG and EA in the liver revealed statistically significant changes on antioxidant enzyme system and malondialdehyde formation.ConclusionThe changes in biomarkers activity indicate a greater production of free radicals which exceeds the capability of antioxidant system, appearing with oxidative stress in the group of animals treated by 4-MP combined with EG and EA.     

Bleomycin toxicity: alterations in oxidative metabolism in lung and liver microsomal fractions

Separate groups of male rats received low doses (5 units) or high doses (15 units) of bleomycin i.p. twice weekly for 1.5, 3 or 6 weeks. The susceptibility of tissue lipid to peroxidation and the activities of mixed function oxidations were examined in microsomal fractions prepared from lung and liver. ADP-Fe (III)-initiated lipid peroxidation was stimulated in lung microsomal fractions only in animals treated with high-dose bleomycin for 1.5 weeks, whereas a 2- to 4-fold enhancement was observed in liver preparations from all bleomycin-treated animals. Microsomal ADP-Fe (III)-initiated lipid peroxidation was inhibited, however, by the in vitro addition of bleomycin in both lung and liver preparations, but this inhibition was an artifact resulting from the chelation of Fe (III) by bleomycin. Soybean lipoxygenase I-initiated microsomal lipid peroxidation, which does not require added iron, was unaffected by bleomycin in lung preparations but was inhibited in liver. Following in vivo treatment, lung microsomal hydrogen peroxide generation was inhibited by 1.5 weeks of high-dose bleomycin treatments, whereas benzphetamine N-demethylation was unchanged. These cytochrome P-450-dependent reactions were both suppressed, however, in liver microsomal fractions. In vitro, both reactions were also inhibited by bleomycin in liver but not in lung microsomal fractions. The lack of effect of in vitro bleomycin treatments on Superoxide generation in lung or liver preparations suggests that the NADPH cytochrome P-450 reductase component of the mixed function oxidase system was not affected. Minimal alterations in lipid peroxidizability and mixed function oxidase activities in lung microsomal fractions of bleomycin-treated animals suggest that the insensitivity could be due to: (1) the site of toxicity not being at the level of the endoplasmic reticulum; or (2) the target of bleomycin toxicity being limited to a small population of pulmonary cell types. Even though the liver is not susceptible to bleomycin toxicity, the hepatic microsomal mixed function oxidase system is highly sensitive to this chemical.     

Effect of grape (Vitis vinifera L.) leaf extract on alcohol induced oxidative stress in rats

Alcoholic liver disease is a major medical complication of drinking alcohol. Oxidative stress plays an important role in the development of alcohol liver disease. The present study was carried to evaluate the effect of grape leaf extract (GLEt) on antioxidant and lipid peroxidation states in liver and kidney alcohol induced toxicity. In vitro studies with DPPH* and ABTS*(+) (cation radical) showed that GLEt possesses antioxidant activity. In vivo administration of ethanol (7.9 g/kg bw/day) for 45 days resulted an activity of liver marker enzymes (AST, ALT, ALP and GGT), lipid peroxidation markers (TBARS, lipid hydroperoxides) in liver and kidney with significantly lower activity of SOD, CAT, GPx, GST and non-enzymatic antioxidants (vitamin E, vitamin C and GSH) in liver and kidney as compared with control rats. Administration of ethanol along with GLEt significantly decreased the activities of liver markers enzyme in serum towards near normal level. GLEt at a dose of 100 mg/kg was highly effective than 25 and 50 mg/kg body weight. In addition GLEt also significantly reduced the levels of lipid peroxidation and addition, significantly restored the enzymic and non-enzymatic antioxidants level in liver and kidney of alcohol administration rats. This observation was supplemented by histopathological examination in liver and kidney. Our data suggest that GLEt exerts its protective effect by decreased the lipid peroxidation and improving antioxidants status, thus proving itself as an effective antioxidant in alcohol induced oxidative damage in rats.     

MAHARISHI AMRIT KALASH REJUVENATES AGEING CENTRAL NERVOUS SYSTEM'S ANTIOXIDANT DEFENCE SYSTEM: AN IN VIVO STUDY

The oxygen-free radical involvement in various deteriorative processes and in ageing is unquestionably established. In the present study age-related changes in antioxidant enzyme activity in the different regions of CNS of 10-month and 32-month-old guinea pigs were studied. Maharishi Amrit Kalash has shown promise in inhibiting the in vitro and in vivo lipid peroxidation. Therefore in the present study the effect of MAK on the activity of antioxidant enzymes was checked. Our results indicate that the activity of superoxide dismutase and glutathione peroxidase, was found to be reduced (P<0.05) in all the regions of CNS studied, The activities of catalase declined significantly only in the cerebral cortex, hypothalamus and the cerebellum. Whereas glutathione reductase activity declined in the cerebral cortex and hypothalamus. It is concluded that the age-related decline in the activities of antioxidant enzymes is region-specific as well as enzyme-specific. The endogenous lipid peroxide was found to be increased significantly (P<0.05) in the 32-month-old animals. Whereas the lipid peroxidation after incubating the tissue homogenate in the air was found to be decreased (P<0.05) in the older animals. The results indicate that the accumulation of lipid peroxides take place with age but the susceptibility of lipid peroxidation decreases in the older animals. The treatment of MAK 500 mg kg⁻¹body wt. for 2 months could augment the activities of antioxidant enzymes (P<0.05). The effect of MAK was more pronounced in older than younger animals. It is concluded that the MAK can be used in compensating the decline in the activities of antioxidant enzymes in CNS and thereby it reduces the risks of lipid peroxidation.pc 1999 Academic Press@p$hr     

An evaluation of antioxidant, anti-inflammatory, and antinociceptive activities of essential oil from Curcuma longa. L

Objectives:

This study was aimed to evaluate the chemical composition, antioxidant potential in vitro and in vivo, anti-inflammatory, and antinociceptive activity of turmeric oil.

Materials and Methods:

Chemical analysis of turmeric oil was done by gas chromatography/mass spectrometry. Antioxidant activities in vitro was done by six different methods and in vivo antioxidant activity was determined by measuring superoxide generation from macrophages treated with phorbol-12-myristate-13-acetate (PMA) as well as determining antioxidant level after feeding the oil orally for one month. Anti-inflammatory activity was studied in mice using carrageenan, dextran, and formalin. Antinociceptive activity was evaluated by using acetic acid-induced writhing movement in mice.

Results:

The main constituent of essential oil of turmeric was found to be ar-turmerone (61.79%), curlone (12.48%), and ar-curcumene (6.11%). Turmeric oil was found to have in vitro antioxidant activity and IC₅₀ for scavenging superoxides, hydroxyl radicals, and lipid peroxidation were 135 μg/ml, 200 μg/ml, and 400 μg/ml, respectively. The ferric-reducing activity for 50 μg of turmeric essential oil was found to be 5 mM. Intraperitoneal administration of oil was found to inhibit PMA-induced superoxide radicals elicited by macrophages. Oral administration of turmeric oil for one month to mice significantly increased superoxide dismutase, glutathione, and glutathione reductase enzyme levels in blood and glutathione-S-transferase and superoxide dismutase enzymes in liver. Turmeric oil showed significant reduction in paw thickness in carrageenan, dextran-induced acute inflammation, and formalin-induced chronic inflammation. The drug produced significant antinociceptive activity (P < 0.001) at all doses studied.

Conclusions:

These results demonstrated that turmeric oil has potential health benefits as it can scavenge the free radicals and produce significant anti-inflammatory and antinociceptive activities.     

Preventive effects of a purified extract isolated from Salvia miltiorrhiza enriched with tanshinone I,tanshinone IIA and cryptotanshinone on hepatocyte injury in vitro and in vivo

Salvia miltiorrhiza is traditionally used to treat liver disease in Asia. In this study, we tested the ability of a purified extract of S. miltiorrhiza (PF2401-SF) and its constituents, tanshinone I, tanshinone IIA, and cryptotanshinone, to protect against acute and subacute liver damage induced by carbon tetrachloride by measuring serum transaminase levels, the reduced form of glutathione (GSH), antioxidant enzyme activities, and lipid peroxidation levels in the liver. We also evaluated their ability to protect primary cultured rat hepatocytes from tertiary-butylhydroperoxide (tBH) or d-galactosamine (GalN). PF2401-SF was protective at 50–200 mg/kg per day in acute liver injury and 25–100 mg/kg per day in subacute liver injury. Tanshinone I, tanshinone IIA, and cryptotanshinon (40 μM), inhibited lactate dehydrogenase leakage, GSH depletion, lipid peroxidation and free radical generation in vitro. PF2401-SF and its major constituents, tanshinone I, tanshinone IIA and cryptotanshinone, can protect against liver toxicity in vivo and in vitro due to its antioxidant effects.