PGE from Octopus aegina Induces Apoptosis in Ehrlich's Ascites Carcinoma of Mice.

ABSTRACT The present study was carried out to assess the antitumor effect of venomous peptide from the cephalopod Octopus aegina on Ehrlich's ascites carcinoma (EAC). Male albino Swiss mice were used in the present study. Four groups of animals were treated with three doses of the sublethal dose of venom, 15, 75, and 150 mug/kg body weight (intraperitoneal injection), along with the standard drug 5-fluorouracil (20 mg/kg b.w.). After 10 days of treatment, six animals from each group were sacrificed for the biochemical analysis and the rest were left to calculate the mean survival time. In EAC-bearing mice, mean lifespan, tumor volume, hemoglobin, red blood cells, and lymphocytes were significantly decreased when compared to the normal animals. While body weight, neutrophils, and viable tumor cell count were increased in the EAC-bearing mice, these changes were brought back to near normal levels in different treatment groups. The macromolecule concentration of peritoneal cells, such as DNA, RNA, and protein, were altered in the EAC-bearing mice and observed to be near normal in the treatment groups. The caspase-3 activity was significantly increased in the peritoneal cells of the treatment groups when compared to the EAC-bearing mice. The role of apoptotic cascade in EAC cell death was confirmed by the DNA fragmentation on agarose gel. Apart from the antitumor effect, octopus venom reduced the tumor burden on the liver and altered the changes in the activities of alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP). Therefore, the venom from O. aegina has a potential antitumor effect on the EAC-bearing mice.

In vivo and in vitro characterization of the biochemical and pathological changes induced by lionfish (pterios volitans) venom in mice.

Accidents caused by lionfish (Pterios volitans) envenomation are characterized by edema, intense pain, and necrosis at the site of sting. The mode of action and biochemistry of venoms are obviously complex and require a better knowledge and investigation to explore the toxic action and resulting biochemical changes. In the present study the LD(50) value of lionfish venom was found to be 42.5 mug/kg body weight (intraperitoneal injection) in Albino Swiss mice and was associated with reduced motor activity and asphyxiation followed by respiratory failure. The effect on vital organs revealed spongiosis in brain, vascular congestion in liver, cloudy swelling of renal tubules, congested blood vessels in renal tubules, and degeneration of myofibrils in heart. Whereas, the 10% of LD(50) (was 4.25 mug/kg b.w.), the sublethal dose showed reversible changes in the hematological (blood cell count, hematocrit, hemoglobin, mean corpuscular volume, mean corpuscular hemoglobin, and platelet count) parameters, serum enzymes (aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase, and creatinine phosphokinase), blood sugar, urea, creatinine, triglycerides, cholesterol, and total protein in mouse in vivo. The in vitro analysis of lionfish venom on mouse brain acetyl cholinesterase and Na(+), K(+), ATPase showed significant increased activity in a dose-dependent manner (10 to 40 mug). Moreover, the lionfish venom was observed to have a protease with a molecular weight of 45 kDa. Hence, the present study suggests the presence of bioactive proteins and peptides with excellent target specificity, which could be trapped for drug development in near future.

Effect of photo-irradiated curcumin treatment against oxidative stress in streptozotocin-induced diabetic rats.

Increasing evidence in both experimental and clinical studies suggests that oxidative stress plays a major role in the pathogenesis of diabetes mellitus. Although phenolic compounds attenuate oxidative stress-related damage, there are concerns over toxicity of synthetic phenolic antioxidants, and this has considerably stimulated interest in investigating the role of natural phenolics in medicinal application. In the present study, we examined the effect of photo-irradiated curcumin in experimental diabetes to evaluate the anti-hyperglycemic properties of this compound on streptozotocin (40 mg/kg of body weight)-induced diabetes. Photo-irradiated curcumin was given at a dose of 10 or 30 mg/kg of body weight. The level of blood glucose was elevated in diabetic animals. Circulatory lipid peroxidation, vitamin C, vitamin E, and enzymic antioxidants such as superoxide dismutase and catalase were analyzed. The antioxidant status decreased in diabetic animals. Oral administration of photo-irradiated curcumin for 45 days resulted in a significant decrease in the levels of blood glucose along with near-normalization of the enzymic activities and the levels of lipid peroxidative markers. The most effective results were obtained on treatment with 30 mg/kg of body weight of photo-irradiated curcumin.

Ferulic acid alleviates lipid peroxidation in diabetic rats.

Diabetes mellitus is a metabolic disorder associated with increased formation of free radicals. The objective of our study was to determine whether ferulic acid (FA), a phenolic acid, has any role to play in diabetes induced free radical formation. Diabetes was induced with streptozotocin. The levels of blood glucose, thiobarbituric acid reactive substances (TBARS), hydroperoxides and free fatty acids (FFA) increased in the liver of diabetic animals. The activities of glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) decreased in the liver. Histopathology of pancreas also shows shrunken islets. Supplementation of FA to the diabetic rats resulted in a decrease in the levels of glucose, TBARS, hydroperoxides, FFA and an increase in reduced glutathione (GSH). FA also resulted in increased activities of SOD, CAT, GPx and expansion of pancreatic islets. The effect was much pronounced with lower dose treatment. Thus our study shows that administration of ferulic acid helps in enhancing the antioxidant capacity of these diabetic animals by neutralizing the free radicals formed thereby reducing the intensity of diabetes.