RESUMEN
Circular dichroism (CD) spectra of photosystem I (PSI) complexes of the cyanobacteria Thermosynechococcus elongatus, Arthrospira platensis and Synechocystis sp. PCC 6803 were studied. CD spectra of dark-adapted PSI trimers and monomers, measured at 77 K, show common bands at 669-670(+), 673(+), 680(-), 683-685(-), 696-697(-), 702(-) and 711(-) nm. The intensities of these bands are species specific. In addition, bands at 683-685(-) and 673(+) nm differ in intensity for trimeric and monomeric PSI complexes. CD difference spectra (P700(+)-P700) of PSI complexes at 283 K exhibit conservative bands at 701(-) and 691(+) nm due to changes in resonance interaction of chlorophylls in the reaction center upon oxidation of P700. Additional bands are observed at 671(-), 678(+), 685(-), 693(-) nm and in the region 720-725 nm those intensities correlate with intensities of analogous bands of antenna chlorophylls in dark-adapted CD spectra. It is suggested that the variability of CD difference spectra of PSI complexes is determined by changes in resonance interaction of reaction center chlorophylls with closely located antenna chlorophylls.
Asunto(s)
Proteínas Bacterianas/metabolismo , Dicroismo Circular , Cianobacterias/metabolismo , Complejos de Proteína Captadores de Luz/metabolismo , Luz , Proteínas Bacterianas/química , Cianobacterias/química , Complejos de Proteína Captadores de Luz/químicaRESUMEN
Effects of oxygen and photosynthesis and respiration inhibitors on the electron transport in photosystem I (PSI) of the cyanobacterium Arthrospira platensis cells were studied. Redox transients of P700 were induced by illumination at 730 nm and monitored as kinetics of the absorption changes at 810 nm; to block electron influx from PSII, the measurements were performed in the presence of 30 microM 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU). Inhibitors of terminal oxidases (potassium cyanide and pentachlorophenol) insignificantly influenced the fast oxidation of P700 under aerobic conditions, whereas removal of oxygen significantly decelerated the accumulation of P700(+). In the absence of oxygen the slow oxidation of P700 observed on the first illumination was accelerated on each subsequent illumination, suggesting an activation of the carbon cycle enzymes. Under the same conditions, pentachlorophenol (an uncoupler) markedly accelerated the P700 photooxidation. Under anaerobic conditions, potassium cyanide (an inhibitor of carbon dioxide assimilation) failed to influence the kinetics of redox transients of P700, whereas iodoacetamide (an inhibitor of NADP(H)-glyceraldehyde-3-phosphate dehydrogenase) completely prevented the photooxidation of P700. Thus, the fast photooxidation of P700 in the A. platensis cells under aerobic conditions in the presence of DCMU was caused by electron transport from PSI onto oxygen, and complicated transient changes in the P700 photooxidation kinetics under anaerobic conditions (in the presence of DCMU) were due to involvement of NADP+ generated during the reducing phase of the carbon cycle.
Asunto(s)
Carbono/metabolismo , Cianobacterias/metabolismo , Oxígeno/farmacología , Fotosíntesis/fisiología , Complejo de Proteína del Fotosistema I/metabolismo , Aerobiosis , Anaerobiosis , Cianobacterias/efectos de los fármacos , Cianobacterias/efectos de la radiación , Diurona/farmacología , Transporte de Electrón/efectos de los fármacos , Transporte de Electrón/efectos de la radiación , Cinética , NADP/metabolismo , Oxidación-Reducción/efectos de los fármacos , Oxidación-Reducción/efectos de la radiación , Oxígeno/metabolismo , Pentaclorofenol/farmacologíaRESUMEN
Induction of cancer by inorganic arsenic occurs inconsistently between species and between routes of exposure, and it exhibits different dose-response relationships between different target organs. Inhaled or ingested arsenic causes cancer in humans but not in other species. Inhaled arsenic primarily induces lung cancer, whereas ingested arsenic induces cancer at multiple sites, including the skin and various other organs. Cancer potency appears to vary by route of exposure (ingestion or inhalation) and by organ site, and increases markedly at higher exposures in some instances. To understand what might explain these inconsistencies, we reviewed several hypotheses about the mechanism of cancer induction by arsenic. Arsenic disposition does not provide satisfactory explanations. Induction of cell proliferation by arsenic is a mechanism of carcinogenesis that is biologically plausible and compatible with differential effects for species or differential dose rates for organ sites. The presence of other carcinogens, or risk modifiers, at levels that correlate with arsenic in drinking water supplies, may be a factor in all three inconsistencies: interspecies specificity, organ sensitivity to route of administration, and organ sensitivity to dose rate.