Development of high-performance supercapacitor electrode derived from sugar industry spent wash waste.

This study aims at developing supercapacitor materials from sugar and distillery industry wastes, thereby mediating waste disposal problem through reuse. In a two-step process, biomethanated spent wash (BMSW) was acid treated to produce solid waste sludge and waste water with significantly reduced total organic carbon (TOC) and biological oxygen demand (BOD) content. Further, waste sludge was directly calcined in presence of activating agent ZnCl2 in inert atmosphere resulting in high surface area (730-900m2g-1) carbon of unique hexagonal morphology. Present technique resulted in achieving two-faceted target of liquid-solid waste remediation and production of high-performance carbon material. The resulted high surface area carbon was tested in both three and two electrode systems. Electrochemical tests viz. cyclic voltammetry, galvanostatic charge-discharge and impedance measurement were carried out in aqueous KOH electrolyte yielding specific capacitance as high as 120Fg-1, whereas all solid supercapacitor devised using PVA/H3PO4 polyelectrolyte showed stable capacitance of 105Fg-1 at 0.2Ag-1. The presence of transition metal particles and hetero-atoms on carbon surface were confirmed by XPS, EDX and TEM analysis which enhanced the conductivity and imparted pseudocapacitance to some extent into the working electrode. The present study successfully demonstrated production of high-performance electrode material from dirtiest wastewater making process green, sustainable and economically viable.

In vitro and in vivo studies on antitumor effects of gossypol on human stomach adenocarcinoma (AGS) cell line and MNNG induced experimental gastric cancer.

The present study has evaluated the chemopreventive effects of gossypol on N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced gastric carcinogenesis and on human gastric adenocarcinoma (AGS) cell line. Gossypol, C(30)H(30)O(8), is a polyphenolic compound that has anti proliferative effect and induces apoptosis in various cancer cells. The aim of this work was to delineate in vivo and in vitro anti-initiating mechanisms of orally administered gossypol in target (stomach) tissues and in human gastric adenocarcinoma (AGS) cell line. In vitro results prove that gossypol has potent cytotoxic effect and inhibit the proliferation of adenocarcinoma (AGS) cell line. In vivo results prove gossypol to be successful in prolonging the survival of MNNG induced cancer bearing animals and in delaying the onset of tumor in animals administrated with gossypol and MNNG simultaneously. Examination of the target (stomach) tissues in sacrificed experimental animals shows that administration of gossypol significantly reduces the level of tumor marker enzyme (carcino embryonic antigen) and pepsin. The level of Nucleic acid contents (DNA and RNA) significantly reduces, and the membrane damage of glycoprotein subsides, in the target tissues of cancer bearing animals, with the administration of gossypol. These data suggest that gossypol may create a beneficial effect in patients with gastric cancer.

Chemopreventive role of sulforaphane by upholding the GSH redox cycle in pre- and post-initiation phases of experimental lung carcinogenesis.

Sulforaphane (SFN) is a natural, biologically active compound extracted from cruciferous vegetables such as broccoli and cabbage with anti-inflammatory and anti-cancer properties. The present study was carried to assess cytoprotective potential in alleviating oxidative stress, to influence the initiation and subsequent carcinogenesis caused by benzo(a)pyrene [B(a)P] administration in the pre- and post-initiation phases of carcinogenesis in Swiss albino mice. Sulforaphane, supplemented orally at a dose of 9µmoles /mouse/day was found to greatly lessen the damaging effects of B(a)P in mice by increasing the availability of reducing equivalents to fulfil the futile GSH redox cycle and replenish GSH biosynthesis, stabilizing the thiol status. Activity of superoxide dismutase and catalase in native gel prove their differential activities in cancer induced and treated animals. SFN was also found to prevent formation of leaky membranes by boosting the antioxidant status leading to maintenance of ATPase activity in B(a)P treated animals. Histopathological analysis confirmed reduction of carcinogen-associated morphological changes in the lung tissue. The results suggest that SFN has potential as a chemopreventive phytochemical against B(a)P induced lung damage in the processes of carcinogenesis.

Protective role of sulforaphane against oxidative stress mediated mitochondrial dysfunction induced by benzo(a)pyrene in female Swiss albino mice.

Recent focus of cancer chemoprevention is on intermediate biomarkers capable of detecting early changes that can be correlated with inhibition of carcinogenic initiation and progression. The present study aimed to delineate in vivo anti-initiating mechanisms of orally administered sulforaphane (SFN) with special reference to mitochondrial dysfunction in target (lungs) and non-target (liver) tissues employing benzo(a)pyrene [B(a)P] as the model carcinogen. The recent revival of interest in the study of mitochondria has been stimulated by the evidence that genetic and/or metabolic alterations in this organelle lead to a variety of human diseases including cancer. These alterations could be either causative or contributing factors. Hence the activities of mitochondrial specific enzymes of TCA cycle and the electron transport complexes were analyzed in the experimental groups to assess the ATP production. Short-term tests such as the assessment of antioxidant status and reactive oxygen species (ROS)-induced lipid peroxidation, are widely used in the detection and evaluation of anticarcinogens. The assessment of mitochondrial lipid peroxidation along with the antioxidant status proved worthy for the correlation to the degree of damage. The induction of cancer was confirmed by the immunohistochemistry for Bcl-2. The results prove sulforaphane to be very successful in combating the oxidative stress mediated mitochondrial dysfunction in experimental lung carcinogenesis induced by benzo(a)pyrene.

Ursolic acid attenuates oxidative stress-mediated hepatocellular carcinoma induction by diethylnitrosamine in male Wistar rats.

Hepatocellular carcinoma is the most common primary cancer of the liver in Asian countries. For more than a decade natural dietary agents including fruits, vegetables and spices have drawn a great deal of attention in the prevention of diseases, preferably cancer. Ursolic acid is a natural triterpenoid widely found in food, medicinal herbs, apple peel and other products it has been extensively studied for its anticancer and antioxidant properties. The purpose of this study was to evaluate the effect of ursolic acid in diethylnitrosamine (DEN) induced and phenobarbital promoted hepatocarcinogenesis in male Wistar rats. Antioxidant status was assessed by alterations in level of lipid peroxides and protein carbonyls. Damage to plasma membranes was assessed by levels of membrane and tissue ATPases. Liver tissue was homogenized and utilized for estimation of lipid peroxides, protein carbonyls and glycoproteins. Anticoagulated blood was utilized for erythrocyte membrane isolation. Oral administration of UA 20 mg/kg bodyweight for 6 weeks decreased the levels of lipid peroxides and protein carbonyls at a significance of p< 0.05. Activities of membrane and tissue ATPases returned to normal after UA administration. Levels of glycoproteins were also restored after treatment. Histopathological observations were recorded. The findings from the above study suggest the effectiveness of UA in reducing the oxidative stress mediated changes in liver of rats. Since UA has been found to be a potent antioxidant, it can be suggested as an excellent chemopreventive agent in overcoming diseases like cancer which are mediated by free radicals.