From our findings we conclude that bacoside A is effective to prevent DEN-induced hepatocellular carcinoma by quenching lipid peroxidation and enhancing antioxidant status through free radical scavenging mechanism and having potential of protecting endogenous enzymatic and non-enzymatic antioxidant activity.

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Cancer metastasis is a complex multi-step process, responsible for a majority of cancer-related deaths by affecting the critical organs and causing complications in therapies. Hepatocellular carcinoma is a multi-factorial disease and is the third most common cause of cancer related mortality worldwide. Clinical and experimental studies have shown that MMP-2 and MMP-9 are involved in tumor invasion and metastases and their elevated expression has been associated with poor prognosis. Our recent studies showed a strong anti-oxidant and hepatoprotective effects of bacoside A (BA) against carcinogen. Nevertheless the effect of BA on the activities and expression of MMP-2 and MMP-9 during hepatocellular carcinoma is not yet recognized. Therefore, the present study was designed to assess the same. Results of gelatin zymography study showed that BA co-treatment significantly decreased the activities of MMP-2 and MMP-9, which is increased during hepatocellular carcinoma. Further immunoblot analysis showed decreased expression of MMP-2 and MMP-9 in rats co-treated with BA compared to DEN-induced hepatocellular carcinoma. Our results reveal that BA exerts its anti-metastatic effect against DEN-induced hepatocellular carcinoma by inhibiting the activities and expressions of MMP-2 and MMP-9.

N-Nitrosodiethylamine (DEN) is a notorious carcinogen, present in many environmental factors. DEN induces oxidative stress and cellular injury due to enhanced generation of reactive oxygen species; free radical scavengers protect the membranes from DEN-induced damage. The present study was designed to evaluate the protective effect of bacoside A (the active principle isolated from Bacopa monniera Linn.) on carcinogen-induced damage in rat liver. Adult male albino rats were pretreated with 15 mg/kg body weight/day of bacoside A orally (for 14 days) and then intoxicated with single necrogenic dose of N-nitrosodiethylamine (200 mg/kg bodyweight, intraperitonially) and maintained for 7 days. The liver weight, lipid peroxidation (LPO), and activity of serum marker enzymes (aspartate transaminases, alanine transaminases, lactate dehydrogenase, alkaline phosphatase, and gamma-glutamyl transpeptidase) were markedly increased in carcinogen-administered rats, whereas the activities of marker enzymes were near normal in bacoside A-pretreated rats. Activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutatione-S-transferase, and reduced glutathione) in liver also decreased in carcinogen-administered rats, which were significantly elevated in bacoside A-pretreated rats. It is concluded that pretreatment of bacoside A prevents the elevation of LPO and activity of serum marker enzymes and maintains the antioxidant system and thus protects the rats from DEN-induced hepatotoxicity.

A study was conducted to determine the kinetics of metabolism of sugarcane in vivo under heat stress. 30-days-old sugarcane settlings (Co 86032) were subjected to critical temperature (40°C) for 5, 10, 15, 20, 25 and 30 h. The metabolic changes in terms of total phenolics, total sugars, proline, glycinebetaine and reactive oxygen species (ROS) scavenging enzymes activity and isozyme pattern were studied at different temperatures. A linear accumulation of soluble sugars, free proline and glycinebetaine (up to 25 h of heat stress treatment) was evident in sugarcane sprouts due to heat stress, although none of these metabolites accumulated under control conditions suggesting their role in osmotic adjustment and thereby in protecting cells from heat damage for short heat stress conditions. Heat stress induced increase in total phenolics content of settlings (44.5-128.5 lg g -1 FW) and callus (37.5-105.1 lg g -1 FW) with the gradual increase of sampling timing (5-25 h) might play a role in the prevention of stress-induced oxidative damage and maintenance of osmotic balance. High temperature stress enhanced the activity of antioxidant enzymes up to 15 h of 40°C temperature stress and after wards declined. Higher degree of expression of peroxidase and superoxide dismutase isoform and their activities lead to protection of cells from oxidative damage under heat stress suggesting that the plants have developed enzymatic control of scavenge ROS under short term stress.