Evaluation of the Prevalence of Oral Mucosal Lesions in a Population of Eastern Coast of South India.

OBJECTIVE/AIM: The aim of this study is to measure the association between oral mucosal lesions (OMLs) and habit of tobacco and alcohol in the population of Guntur city, Andhra Pradesh, South India. MATERIAL AND METHOD: A cross-sectional study was conducted on 300 participants in Guntur city with the habit of tobacco and alcohol consumption in various forms who were selected by stratified cluster random sampling technique. Guntur city was divided into four zones, that is, North, East, South, and West; and two administrative wards were randomly selected from each zone as clusters. Information was obtained by interviewing the participant regarding various tobacco-related habits followed by standardized clinical examination in the field. Clinical data were collected using a modified 1980 WHO Pro forma where the basis for diagnosis was established as per the criteria provided by the epidemiology guide for the diagnosis of oral mucosal diseases (WHO). Statistical tests such as Pearson Chi-square were exercised to test the significance, using SPSS version 19.0 with 0.05 as cutoff level of significance. RESULTS: Overall oral soft-tissue lesions were found in 42.4% of the study participants including nicotinic stomatitis, tobacco pouch keratosis, smokers melanosis, mild keratosis of the palate, and chewer's mucosa. In this study, nicotinic stomatitis was found to be the most common soft-tissue lesion among men, while leukoplakia was found to be the most common premalignant lesion with the prevalence being 5.7%. While oral submucous fibrosis was found to be the most common premalignant condition among women. It was found that 13.2% of illiterates (53) were having leukoplakia. In the present study, the lower labial mucosa and buccal mucosa were found to be the most common sites of occurrence of leukoplakia and oral submucous fibrosis. CONCLUSION: This study gives information on the association of OML in smokers, chewers, alcoholics, and those with mixed habits. This study highlighted six habit-related OML which included potentially malignant disorders such as leukoplakia and oral submucous fibrosis. Future case-control or cohort studies for individual lesions and with larger sample size are necessary to evaluate the risk for OML including potentially malignant conditions and oral cancer resulting from smoking and chewing habits.

Capsaicin provokes apoptosis and restricts benzo(a)pyrene induced lung tumorigenesis in Swiss albino mice.

Capsaicin (CAP), a constituent of red chilli and red pepper is exposed to exert compelling anticarcinogenic effects. In the present study, we examined the anti-tumorigenic potential of CAP on benzo(a)pyrene-induced mice lung tumorigenesis by analyzing the markers of apoptosis. Intraperitoneal administration of CAP (10mg/kg body weight) to Swiss albino mice suppressed the development of lung carcinoma by amending the protein expressions of apoptotic regulators p53, Bcl-2, Bax and caspase-3. The apoptotic-inducing nature of CAP was further confirmed by DNA agarose gel electrophoresis, transmission electron microscopic study and ethidium bromide/acridine orange staining. The results obtained from the present study show that CAP inhibits the development of mice lung carcinogenesis through its ability to induce apoptosis. Our present findings provide the basis for further clinical exploration of CAP as an anti-carcinogenic compound against lung carcinogenesis.

Capsaicin inhibits benzo(a)pyrene-induced lung carcinogenesis in an in vivo mouse model.

OBJECTIVE: Lung cancer is a serious health problem in most developed countries and its incidence rate is profusely increasing. Capsaicin, a component of red chilli and red pepper has been studied widely for its chemopreventive properties. The aim of the present study is to explore the anti-tumor activity of capsaicin against benzo(a)pyrene-induced lung tumorigenesis in Swiss albino mice. MATERIALS AND METHODS: Benzo(a)pyrene was administered orally (50 mg/kg body weight) to induce lung cancer in Swiss albino mice. Hematological study (hemoglobin content, RBC, WBC count and differential count), histochemical analysis of mast cells and Western blot analysis of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), cyclooxygenase-2 (COX-2) and nuclear factor-kappa B (NF-κB) were carried out. RESULTS: Hematological parameters and the histochemical analysis of mast cells showed abnormal changes, and the immunoblotting analysis revealed increased protein expression of TNF-α, IL-6, COX-2 and NF-κB in lung cancer-challenged mice administered with benzo(a)pyrene. Capsaicin (10 mg/kg body weight) supplementation to lung cancer bearing mice considerably prevented all the above abnormalities. CONCLUSION: The results of the present study indicate the protective effect of capsaicin against benzo(a)pyrene-induced lung carcinogenesis in mice.

Hepatic perturbations provoked by azathioprine: a paradigm to rationalize the cytoprotective potential of Ficus hispida Linn.

The present study was embarked upon in an endeavor to ascertain whether Ficus hispida leaf extract (FHLE) modulates azathioprine-induced hepatic damage. Azathioprine treated rats displayed a plethora of pathological events, which include loss of hepatocellular membrane integrity, mitochondrial dysfunction, and nuclear damage; whilst FHLE pretreated rats significantly precluded these abnormalities. These data were in harmony with the transmission electron microscopic studies. Observations from this investigation directed us to propose the plausible mechanisms through which FHLE thwarts the repercussions of azathioprine-induced hepatocellular necrosis: upholding of thiol homeostasis, curtailing the membrane effects, and perpetuation of adenine nucleotide status. These data offer credence to the notion that FHLE might be a beneficial intervention in the prevention of hepatotoxicity in azathioprine therapy.

Effect of capsaicin on glucose metabolism studied in experimental lung carcinogenesis.

In the present study, we have assessed the chemopreventive effect of capsaicin (CAP) on glucose metabolism with reference to blood glucose and liver glycogen levels, key glycolytic, and gluconeogenic enzymes along with electron transport chain (ETC) complexes during benzo(a)pyrene (B(a)P)-induced lung cancer in Swiss albino mice. B(a)P (50 mg kg(-1) body weight)-induced lung cancer animals showed marked decline in blood glucose levels, glycogen levels, elevations in the activities of key glycolytic enzymes (hexokinase, phosphoglucoisomerase and aldolase), and gluconeogenic enzymes (glucose-6-phosphatase and fructose-6-phosphatase) together with a decrease in the activities of ETC complexes. Supplementation of CAP (10 mg kg(-1) body weight) inhibited all the above alterations during lung cancer and restored near normalcy. Histochemical analysis by periodic acid Schiff's staining further confirmed the biochemical findings that highlighted the chemopreventive action of CAP during B(a)P-induced experimental lung tumourigenesis.

Capsaicin alleviates the imbalance in xenobiotic metabolizing enzymes and tumor markers during experimental lung tumorigenesis.

Lung cancer is currently a leading cause of death all over the world. Environmental risk factors, particularly genotoxic chemicals such as polycyclic aromatic hydrocarbons (PAH), are likely to account for a much higher mortality. Xenobiotic metabolizing enzymes are potentially chief determinants in both the susceptibility to the mutagenic effects of chemical carcinogens and in the response of tumors to chemotherapy. The well-known carcinogen benzo(a)pyrene (B(a)P) of PAH family was given orally (50 mg/kg body weight) to induce lung cancer in Swiss albino mice. B(a)P induction altered the levels of cytochromes (P450, b5), activities of phase I biotransformation enzymes (NADPH-cytochrome P450 reductase, NADH-cytochrome b5 reductase and epoxide hydrolase), phase II enzymes (glutathione-S-transferase, UDP-glucuronyl transferase and DT-diaphorase), and the levels of serum tumor markers. Treatment with capsaicin (CAP) (10 mg/kg body weight) to the lung carcinoma mice restored back the activities of phase I and II biotransformation enzymes and the levels of tumor markers to near normalcy. The above findings were substantiated by immunoblotting and immunohistochemical analysis of cytochrome P450 1A1 (CYP1A1) in the lung tissues. Our present study unravels that CAP can effectively detoxify the carcinogens which discloses its anti-carcinogenic effect during experimental lung cancer.

Silymarin inhibited proliferation and induced apoptosis in hepatic cancer cells.

OBJECTIVES: The aim of this study was to investigate mechanisms involved in the growth inhibitory effect of silymarin, in humanhepatocellular carcinoma. MATERIALS AND METHODS: The human hepatocellular carcinoma cell line HepG2 was utilized and the MTT assay was performed to study the antiproliferative effect of silymarin. Dual staining was undertaken for ethidium bromide/acridine orange, propidium iodide staining and DNA fragmentation studies were executed to confirm the presence of apoptosis. Cell-cycle analysis was revealed by flow cytometry and mitochondrial transmembrane potential was measured by uptake of the mitochondrial-specific lipophilic cationic dye rhodamine 123. Western blotting analysis for cytochrome c, p53, Bax, Bcl-2, APAF-1, caspase-3, survivin, beta-catenin, cyclin D1, c-Myc and PCNA was carried out. RESULTS: Silymarin inhibited population growth of the hepatocellular carcinoma cells in a dose-dependent manner, and the percentage of apoptotic cells was increased after treatment with 50 and 75 microg/ml silymarin for 24 h. Silymarin treatment increased the proportion of cells with reduced DNA content (sub-G(0)/G(1) or A(0) peak), indicative of apoptosis with loss of cells in the G(1) phase. Silymarin also decreased mitochondrial transmembrane potential of the cells, thereby increasing levels of cytosolic cytochrome c while up-regulating expression of pro-apoptotic proteins (such as p53, Bax, APAF-1 and caspase-3) with concomitant decrease in anti-apoptotic proteins (Bcl-2 and survivin) and proliferation-associated proteins (beta-catenin, cyclin D1, c-Myc and PCNA). CONCLUSIONS: Our results demonstrate that silymarin treatment inhibited proliferation and induced apoptosis in the human hepatocellular carcinoma cell line HepG2.

Ameliorating effect of capsaicin on alterations in lipid metabolism during mice lung carcinoma.

Spices and vegetables possess antioxidant activity that can be applied for preservation of lipids and lower lipid peroxidation in biological systems. In the present study, we have investigated the effect of capsaicin on lipid metabolism during benzo(a)pyrene induced lung cancer in Swiss albino mice. Benzo(a)pyrene (50 mg/kg wt) induced lung cancer animals showed abnormal changes in the tissue and serum lipids, lipoproteins and lipid metabolizing enzymes. Treatment with capsaicin (10 mg/kg body wt) remarkably attenuated all the above alterations and restored normalcy. These findings reveal the chemomodulatory potential of capsaicin in attenuating the alterations in lipid metabolism during experimental lung carcinogenesis.

Lysosomal abnormalities during benzo(a)pyrene-induced experimental lung carcinogenesis--defensive role of capsaicin.

The objective of the present study was to investigate whether lysosome is a target in benzo(a)pyrene-induced, oxidative stress-mediated lung cancer in Swiss albino mice and the plausible role of the phytochemical substance capsaicin in mitigating lysosomal damage. Oxidative stress was assessed based on the level of carbonyl content. The activities of lysosomal proteases like cathepsin-D, cathepsin-B, beta-D-glucosidase, beta-D-galactosidase, beta-D-glucuronidase, beta-D-N-acetylglucosaminidase and acid phosphatase were assessed to evaluate lysosomal function. Administration of benzo(a)pyrene (50 mg/kg body weight) to mice induced a increase in the activities of lysosomal enzymes and oxidative stress was evident by the increase in carbonyl content. Treatment with capsaicin (10 mg/kg body weight) decreased carbonyl content and restored the activities of lysosomal enzymes to near normalcy. Transmission electron microscopic study of lysosomes further showed the defensive action of capsaicin against the lysosomal damage caused in benzo(a)pyrene-induced lung cancer. From the present study, it can be concluded that lysosomal damage is an indispensable event in benzo(a)pyrene-induced lung cancer, and capsaicin was able to effectively prevent it, which proves the chemoprotective effect of capsaicin against benzo(a)pyrene-induced experimental lung carcinogenesis.

Beneficial influence of capsaicin on lipid peroxidation, membrane-bound enzymes and glycoprotein profile during experimental lung carcinogenesis.

This study was designed to examine the impact of a principal component of hot red peppers and chilli peppers, capsaicin, on alterations in lipid peroxidation, membrane-bound enzyme profiles and glycoprotein levels during benzo(a)pyrene (BP)-induced lung cancer in Swiss albino mice. BP (50 mgkg(-1)) induced deleterious changes that were that revealed by alterations in lipid peroxidation, membrane-bound enzyme (Na+/K+ ATPase, Ca2+ ATPase and Mg2+ ATPase) activity, levels of total protein and protein-bound carbohydrate components (sialic acid, hexose, hexosamine, hexuronic acid and fucose). Pre-co-treatment with capsaicin (10 mg kg(-1)) restored the detrimental effects induced by BP, indicating its protective role in BP-induced lung cancer.

Capsaicin modulates pulmonary antioxidant defense system during benzo(a)pyrene-induced lung cancer in Swiss albino mice.

The effect of a pungent ingredient of red pepper, capsaicin, on oxidative stress induced changes in the antioxidant defense system by benzo(a)pyrene in the lungs of mice was studied. Oral gavage administration of benzo(a)pyrene (50 mg/kg body weight) to mice led to a marked increase in oxidative stress indicated by alterations in pulmonary lipid peroxidation, enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase) and non-enzymic antioxidants (reduced glutathione, vitamin C, vitamin E and vitamin A). Pre-co-treatment with capsaicin (10 mg/kg body weight i.p.) restored cellular normalcy, highlighting the antioxidant potential of capsaicin in mitigating the oxidative stress mediated damage produced during benzo(a)pyrene-induced lung cancer.

Stabilization of pulmonary mitochondrial enzyme system by capsaicin during benzo(a)pyrene induced experimental lung cancer.

The modulatory efficacy of capsaicin on lung mitochondrial enzyme system with reference to mitochondrial lipid peroxidation (LPO), antioxidants, key citric acid cycle enzymes and respiratory chain enzymes during benzo(a)pyrene (B(a)P) induced lung cancer in Swiss albino mice was studied. Elevations in mitochondrial LPO along with decrements in enzymic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST)), non-enzymic antioxidants (reduced glutathione (GSH), vitamin C, vitamin E and vitamin A), citric acid cycle enzymes (isocitrate dehydrogenase (ICDH), alpha-ketoglutarate dehydrogenase (alpha-KDH), succinate dehydrogenase (SDH) and malate dehydrogenase (MDH)), and respiratory chain enzymes (NADH dehydrogenase and Cytochrome c oxidase) were observed in B(a)P (50mg/kg body weight) administered animals. CAP (10mg/kg body weight) pretreatment decreased lung mitochondrial LPO and augmented the activities of enzymic, non-enzymic antioxidants, citric acid cycle enzymes and respiratory chain enzymes to near normalcy revealing its chemoprotective function during B(a)P induced lung cancer.

Biochemical study on the protective potential of Nardostachys jatamansi extract on lipid profile and lipid metabolizing enzymes in doxorubicin intoxicated rats.

Nardostachys jatamansi is a medicinally important herb of Indian origin used for centuries in Ayurvedic and Unani systems of medicine for the treatment of various ailments. The aim of the present work is to evaluate the effect of ethanolic extract of Nardostachys jatamansi rhizomes on doxorubicin induced myocardial injury with respect to lipid metabolism in serum and heart of Wistar albino rats. Altered lipid metabolism alters the cardiac function which is mainly due to changes in the property of the cardiac cell membrane. Doxorubicin exhibits cardiotoxicity by inhibition of fatty acid oxidation in the heart. The rats treated with a single dose of doxorubicin (15 mg/kg) intraperitoneally showed an increase in serum and cardiac lipids (cholesterol, triglycerides, free fatty acids and phospholipids), along with a significant rise in serum low density lipoproteins (LDL), very low density lipoproteins (VLDL) and drop in high density lipoproteins (HDL) levels, resulting in alteration of serum and cardiac lipid metabolizing enzymes. Pretreatment with a extract of Nardostachys jatamansi (500 mg/kg) orally for seven days to doxorubicin induced rats showed a significant prevention in the lipid status with the activities of the lipid metabolizing enzymes. Histopathological observations were also in correlation with the biochemical parameters. These findings suggest that the protective and hypolipidemic effect of Nardostachys jatamansi against doxorubicin induced myocardial injury in rats could possibly be mediated through its anti lipid peroxidative properties.

Effect of silymarin on N-nitrosodiethylamine induced hepatocarcinogenesis in rats.

AIM: To study the effect of silymarin on the levels of tumor markers and MDA (malondialdehyde)-DNA adduct formation during N-nitrosodiethylamine induced hepatocellular carcinoma in male Wistar albino rats. METHODS: The levels of AFP, CEA and activities of liver marker enzymes in serum, MDA-DNA immunohistochemistry were done according to standard procedures in the control and experimental groups of rats. RESULTS: Hepatocellular carcinoma was evidenced from significant (p < 0.05) increases of alpha-fetoprotein, carcinoembryonic antigen, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, acid phosphatase, lactate dehydrogenase, gamma-glutamyltransferase and 5'-nucleotidase in serum and increased MDA-DNA adducts were also observed in the tissue sections of hepatocellular carcinoma. Silymarin treatment significantly attenuated the alteration of these markers and decreased the levels of MDA-DNA adduct formation. CONCLUSION: Silymarin could be developed as a promising chemotherapeutic adjuvant for the treatment of liver cancer.

Efficacy of Sargassum polycystum (Phaeophyceae) sulphated polysaccharide against paracetamol-induced DNA fragmentation and modulation of membrane-bound phosphatases during toxic hepatitis.

1. The aim of the present study was to assess the protective effect of Sargassum polycystum (sulphated polysaccharide) extract against paracetamol-induced DNA strand breaks and modulation of membrane-bound phosphatases, protein thiols and inorganic cations during toxic hepatitis. 2. Seaweed extract (200 mg/kg per day for 21 days) was administered to male Wistar rats against paracetamol challenge. Serum and liver tissues were used to assess levels of ATPase, protein thiols and inorganic cations using atomic absorption spectroscopy. The fragmentation of DNA was assessed by agarose gel electrophoresis. 3. Paracetamol induced intracellular stress, accompanied by changes in the structural and functional characteristics of liver cell membranes, which affected DNA integrity, membrane-bound ATPase and inorganic cations homeostasis. Rats intoxicated with paracetamol (800 mg/kg, i.p.) showed significant impairment in activities of total ATPase, Mg2+-ATPase, Ca+-ATPase and Na+/K+-ATPase, with concomitant changes in the levels of tissue protein thiols and inorganic cations, such as Na+, K+ and Ca2+. These changes were prevented in animals pretreated with S. polycystum extract, which indicates that S. polycystum supplementation could exert some protective effect against paracetamol-induced toxic hepatitis in rats. 4. The protective effect of the seaweed extract may be due to the presence of sulphated compounds that have free radical-scavenging activity.

Adriamycin induced myocardial failure in rats: protective role of Centella asiatica.

Generation of reactive oxygen species and mitochondrial dysfunction has been implicated in adriamycin induced cardiotoxicity. Mitochondrial dysfunction is characterized by the accumulation of oxidized lipids, proteins and DNA, leading to disorganization of mitochondrial structure and systolic failure. The present study was aimed to evaluate the efficacy of Centella asiatica on the mitochondrial enzymes; mitochondrial antioxidant status in adriamycin induced myocardial injury. Adriamycin (2.5 mg/kg body wt., i.p.) induced mitochondrial damage in rats was assessed in terms of decreased activities (p<0.05) of cardiac marker enzymes (lactate dehydrogenase, creatine phosphokinase, amino transferases), TCA cycle enzymes (isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, malate dehydrogenase, respiratory marker enzymes (NADH-dehydrogenase, cytochrome-C-oxidase), mitochondrial antioxidant enzymes (GPx, GSH, SOD,CAT) and increased (p<0.05) level of lipid peroxidation. Mitochondrial damage was confirmed by transmission electron microscopic examination. Pre-co-treatment with aqueous extract of Centella asiatica (200 mg/kg body wt, oral) effectively counteracted the alterations in mitochondrial enzymes and mitochondrial defense system. In addition, transmission electron microscopy study confirms the restoration of cellular normalcy and accredits the cytoprotective role of Centella asiatica against adriamycin induced myocardial injury. Our results demonstrated elevated oxidative stress and mitochondrial dysfunction in adriamycin treated rats. Moreover, on the basis of our findings it may be concluded that the aqueous extract of C. asiatica not only possesses antioxidant properties but it may also reduce the extent of mitochondrial damage.

Defensive nature of Sargassum polycystum (Brown alga) against acetaminophen-induced toxic hepatitis in rats: role of drug metabolizing microsomal enzyme system, tumor necrosis factor-alpha and fate of liver cell structural integrity.

AIM: To assess the defensive nature of Sargassum polycystum (S. polycystum) (Brown alga) against acetaminophen (AAP)-induced changes in drug metabolizing microsomal enzyme system, tumor necrosis factor (TNF-alpha) and fine structural features of the liver during toxic hepatitis in rats. METHODS: Male albino Wistar strain rats used for the study were randomly categorized into 4 groups. Group I consisted of normal control rats fed with standard diet. Group II rats were administered with acetaminophen (800 mg/kg body weight, intraperitoneally). Group III rats were pre-treated with S. polycystum extract alone. Group IV rats were orally pre-treated with S. polycystum extract (200 mg/kg body weight for 21 d) prior to acetaminophen induction (800 mg/kg body weight, intraperitoneally). Serum separated and liver was excised and microsomal fraction was isolated for assaying cytochrome P450, NADPH Cyt P450 reductase and b(5). Serum TNF-alpha was detected using ELISA. Fine structural features of liver were examined by transmission electron microscopy. RESULTS: Rats intoxicated with acetaminophen showed considerable impairment in the activities of drug metabolizing microsomal enzymes, such as cytochrome P450, NADPH Cyt P450 reductase and b(5) when compared with the control rats. The rats intoxicated with acetaminophen also significantly triggered serum TNF-alpha when compared with the control rats. These severe alterations in the drug metabolizing enzymes were appreciably prevented in the rats pretreated with S. polycystum. The rats pretreated with S. polycystum showed considerable inhibition in the elevation of TNF-alpha compared to the rats intoxicated with acetaminophen. The electron microscopic observation showed considerable loss of structural integrity of the endoplasmic reticulum, lipid infiltration and ballooning of mitochondria in the acetaminophen-intoxicated rats, whereas the rats treated with S. polycystum showed considerable protection against acetaminophen-induced alterations in structural integrity. CONCLUSION: These observations suggest that the animals treated with S. polycystum extract may have the ability to protect the drug metabolizing enzyme system and mitochondrial functional status from free radical attack, thereby showing its defense mechanism in protecting hepatic cells from acetaminophen toxic metabolite N-acetyl-para-benzoquinone-imine (NAPQI).

Protective effect of Premna tomentosa extract (L. verbanacae) on acetaminophen-induced mitochondrial dysfunction in rats.

Allurement of herbs as health beneficial foods (physiologically functional foods) and as a source material for the development of new drugs, has led to greater furtherance in the study of herbal medicines during recent years. Plant extracts are being utilized to treat a wide variety of diseases like hepatotoxicity. Premna tomentosa is one such medicinal plant used widely in Indian ayurvedic medicine for the treatment of liver disorders. This study appraised the effectiveness of P. tomentosa leaf extract in protecting the liver against mitochondrial damage induced by acetaminophen, since mitochondrial injury has been investigated as a potential initiator of hepatotoxicity. Normal Wistar strain rats were pre-treated with P. tomentosa extract (750 mg/kg, orally) for 15 days and then intoxicated with acetaminophen (640 mg/kg, orally). Mitochondria were isolated from liver of experimental animals and assessed for the levels of lipid peroxide products, GSH and mitochondrial enzymes (isocitrate dehydrogenase, alpha-keto glutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, NADH dehydrogenase and cytochrome-C-oxidase). The levels of Lipid peroxidation products were increased and the levels of the other assessed parameters were significantly decreased in hepatotoxicity induced animals. Whereas, the levels were brought back to normal in P. tomentosa pre-treated rats, which shows the protective effect of the extract against mitochondrial damage. Presence of anti-oxidant compound D-limonene (58%) in P. tomentosa leaves, which is known to enhance conjugation of toxic metabolites by maintaining liver GSH concentrations may explain the hepatoprotective property of the extract.

Protective effect of Centella asiatica on antioxidant tissue defense system against adriamycin induced cardiomyopathy in rats.

Increased oxidative stress and antioxidant deficit have been suggested to play a major role in adriamycin induced cardiomyopathy and congestive heart failure due to multiple treatments with adriamycin. In this study the cardio protective effect of Centella asiatica on myocardial marker enzymes and antioxidant enzymes in adriamycin induced cardiomyopathy was investigated in rats. The rats administered with adriamycin (2.5 mg/kg body wt, i.p) caused myocardial damage that was manifested by the elevation of serum marker (LDH, CPK, GOT and GPT) enzymes and showed significant changes in the antioxidant enzymes (SOD, CAT, GPx, GST). Pre-co-treatment with Centella asiatica(200 mg/kg of body wt/oral) extract significantly prevented these alterations and restored the enzyme activities to near normal levels. These findings demonstrate the cardio protective effect of Centella asiatica on antioxidant tissue defense system during adriamycin induced cardiac damage in rats.

Evaluation of the protective efficacy of Asteracantha longifolia on acetaminophen-induced liver damage in rats.

The effect of oral administration of methanolic extract of Asteracantha longifolia (AL) seeds on acetaminophen (APAP)-induced acute liver damage in rats was investigated. The activities of marker enzymes (aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase, and gamma glutamyl transferase) and bilirubin level in serum and the levels of cholesterol, triglycerides, and free fatty acids in both serum and liver were found to be increased when rats were challenged with APAP. This was also associated with a significant reduction of serum and tissue phospholipids. Pretreatment with AL extract prior to the administration of APAP prevented these alterations as evidenced by liver histopathology. Results indicated that the extract could offer protection against APAP-induced liver damage, suggesting its hepatoprotective activity.