Biodiversity of algae and protozoa in a natural waste stabilization pond: a field study.

A field study was carried out on the biodiversity of protozoa and algae from a natural waste stabilization pond during November, 1996 to April, 1997. The raw waste and pond samples were analysed for physico-chemical and biological parameters. High dissolved oxygen (DO) coinciding with phytoplankton peak was recorded. The algae--Chlorella vulgaris, Scenedesmus acuminatus, Oscillatoria brevis and Nostoc piscinale and Protozoa--Paramecium caudatum, Acanthamoeba sp., Bodo saltans and Oikomonas termo were obvious as dominant species, whereas algae Ochromonas pyriformis and Synura uvella and protozoa, Didinium masutum and Stentor coerulus were noted as rare species. Totally 71 species of algae and 13 species of protozoa were identified.

Induction of interleukin-6 by coal containing bioavailable iron is through both hydroxyl radical and ferryl species.

Coal mining causes health problems, such as pneumoconiosis. We have previously shown that prevalence of pneumoconiosis in workers from various coalmine regions positively correlates with levels of bioavailable iron (BAI) in the coals from that region. In the present study, the nature of reactive oxygen species formed by BAI in the coals and its mechanisms of the induction of biological responses were investigated. Human lung epithelial cell line, A549 cells, were used to examine the induction of interleukin-6 (IL-6), a pro-inflammatory cytokine, which is known to play a crucial role in the development of pneumoconiosis. We found that levels of IL-6 protein as well as its mRNA were significantly increased in the cells treated for 24 h with 20 microg/cm2 of the BAI-containing Pennsylvania (PA) coal; for example we observed 6.7-fold increase in IL-6 protein. Levels of IL-6 protein in cells treated with the Utah (UT) coal containing low-BAI were only 1.9-fold of the control levels. The enhancing effect on the IL-6 by the PA coal was similar to that caused by hydrogen peroxide. Superoxide dismutase (SOD), catalase (CAT), and N-acetyl-L-cysteine (NAC) all had inhibitory effects on the PA coal-induced IL-6 formation. However, CAT had the least protective effect as compared to SOD and NAC. Our results indicate that BAI in the PA coal may induce IL-6 through both ferryl species (via iron autoxidation) and hydroxyl radicals (via the Fenton/Haber Weiss reactions).

Cadmium toxicity induced changes in plant water relations and oxidative metabolism of Brassica juncea L. plants.

Excess of cadmium (Cd) induced changes in oxidative scenario and water status of plants viz.., total water content, specific water content, water saturation deficit (WSD) and transpiration of Brassica juncea plants grown in soil pot culture. Although lower and marginal levels of excess cadmium (100 and 250 ppm) improved growth but higher levels (500 ppm) caused significant suppression. Significant accumulation of proline, an indicator of water stress, occurred at higher level of Cd. Gradual increases in activities of certain antioxidant enzymes such as catalase and peroxidase along with increased lipid peroxidation are suggestive of disturbed oxidative metabolism. Taking together, the deleterious effects of Cd and its effects on oxidative metabolism clearly indicate enhanced generation of reactive oxygen species (ROS) to be instrumental in producing toxic effects of Cd. The excess levels of Cd also decreased the concentrations of soluble protein and chlorophylls and increased the ratio of chlorophyll a/b.

Hydrogen Peroxide-Induced Cell Death in a Human Retinal Pigment Epithelial Cell Line, ARPE-19

The loss of retinal pigment epithelium (RPE) with aging is related to age-related macular degeneration (AMD). This study was conducted to investigate the mechanism of hydrogen peroxide (H2O2) induced cell death in a human retinal pigment epithelial cell line, ARPE-19. Hydrogen peroxide was added at different concentrations to ARPE-19 cells and cultured. The cytotoxicity was assayed by mitochondrial function using 3- (4, 5-dimethylthiazol-2-yl) -2, 5-diphenyl tetrazolium bromide (MTT) testing. The patterns of cell damage were assessed using an acridine orange-ethidium bromide differential staining method, in situ end labeling (ISEL) assay and transmission electron microscopy (TEM). Catalase, a major antioxidant, was used to prevent cell death. The cleavage of procaspase 3 and poly (ADP-ribose) polymerase (PARP) was determined by western blot analysis. Hydrogen peroxide significantly induced cell death in ARPE-19 cells, whereas pretreatment of the cells with catalase prevented cell death. Application of the ISEL assay and acridine orange/ethidium bromide staining demonstrated that the H2O2-induced cell death occurred by an apoptotic mechanism at lower concentrations of H2O2 (400, 500, 600 microM), whereas higher concentrations of H2O2 induced necrosis rather than apoptosis. Caspase 3 was associated with the apoptotic pathway in human RPE cell death. Western blot analysis confirmed caspase 3 activation and cleavage of substrate proteins in ARPE-19 cells treated with an H2O2 concentration of 600 microM. These results indicate that treatment with H2O2 induces apoptotic and necrotic cell death in ARPE-19, and that caspase 3 is associated with apoptotic cell death. Therefore, H2O2 may induce the destruction of RPE cells in AMD by the combined effects of apoptosis and necrosis.

Ascorbate induced cross-linking of oxyhemoglobin subunits.

Ascorbic acid during oxidation in vitro can generate H2O2 which induces non-disulphide covalent cross-linking of coincubated oxyhemoglobin. The cross-linking phenomenon mediated by H2O2 takes place possibly without the involvement of hydroxyl radicals as evident from the failure of radical scavengers like mannitol and dimethyl sulphoxide as well as metal-chelator, to inhibit the process. This pro-oxidant effect of ascorbic acid may have physiological significance in red blood cells in vivo.

Cinnabarin synthesis by "Pycnoporus sanguineus" strains antimicrobial astivity against bacteria from food products

Among three strains of "Pycnosporus sanguineus", MIP 89007 produced more cinnabarin than MIP 95001 and MIP 95002. The antimicrobial activity of cinnabarin was tesred against 11 species of bacteria isolated from food. "Bacillus cereus" and "Leuconostoc plantarum" were the most sensitive to cinnabarin, being inhibited by 0.0625 mg/ml. "Klebsiella pneumonia" was the least sensitive (>4.0 mg/ml).

The effects of oxygen radicals on the activity of nitric oxide synthase and guanylate cyclase

Reactive oxygen species such as superoxides, hydrogen peroxide (H2O2) and hydroxyl radicals have been suggested to be involved in the catalytic action of nitric oxide synthase (NOS) to produce NO from L-arginine. An examination was conducted on the effects of oxygen radical scavengers and oxygen radical-generating systems on the activity of neuronal NOS and guanylate cyclase (GC) in rat brains and NOS from the activated murine macrophage cell line J774. Catalase and superoxide dismutase (SOD) showed no significant effects on NOS or GC activity. Nitroblue tetrazolium (NBT, known as a superoxide radical scavenger) and peroxidase (POD) inhibited NOS, but their inhibitory actions were removed by increasing the concentration of arginine or NADPH respectively, in the reaction mixture. NOS and NO-dependent GC were inactivated by ascorbate/FeSO4 (a metal-catalyzed oxidation system), 2'2'-azobis-amidinopropane (a peroxy radical producer), and xanthine/xanthine oxidase (a superoxide generating system). The effects of oxygen radicals or antioxidants on the two isoforms of NOS were almost similar. However, H2O2 activated GC in a dose-dependent manner from 100 microM to 1 mM without significant effects on NOS. H2O2-induced GC activation was blocked by catalase. These results suggested that oxygen radicals inhibited NOS and GC, but H2O2 could activate GC directly.

Superóxido dismutasa más catalasa disminuyen el tamaño del infarto miocárdico en perros / Superoxide dismutase more caralase decrease the size of the myocardial infarct in dogs

Los radicales libres derivados del oxígeno han sido postulados como mediadores en el daño miocárdico inducido por isquemia seguida de reperfusión. Nosotros evaluamos la utilidad de las enzimas depuradoras de radicales libres: superóxido dismutasa (SOD) y catalasa (CAT), para proteger de este daño. En 16 perros anestesiados, a toráx abierto, se ocluyó la arteria coronaria circunfleja durante 90 minutos y se reperfundió por 6 horas. Se estudiaron dos grupos: Grupo A (n=8), que recibió SOD más CAT 0,25 mg de c/u por vía intracoronaria, desde cinco minutoa antes de la oclusión hasta 45 minutos de iniciada la reperfusión. Grupo B (n=8), que recibió solución salina 0,9 por ciento en igual forma. Las áreas de riesgo y necrosada sedelimitaron con tinción con Azul de Evans y Trifeniltetrazolium y se midieron por planimetría. Se registraron presión ventricular izquierda (VI), dp/dt VI y presión aórtica. Se determinaron la longitud y acortamiento segmentario tanto en la zona sometida o no a isquemia mediante cristales piezoeléctricos. El Grupo A presentó una necrosis significativamente menor, cuantificada como porcentaje de área en riesgo (16ñ5 vs 34ñ6 por ciento ; p 0,0001); este efecto fue más significativo en el sentido transmural que lateral. No existieron diferencias entre las áreas en riesgo ni en las variables hemodinámicas entre los grupos. La conclusión, la SOD más CAT reducen el daño miocárdico producido por isquemia seguida de reperfusión, apoyando la hipótesis que los radicales libres participan en la patogenia de este daño