Towards a higher photostability of ZnO photo-electrocatalysts in the degradation of organics by using MMO substrates.
2区 · 环境科学与生态学
作者: Lorena A Goulart ; Géssica O S Santos ; Katlin I B Eguiluz ; Giancarlo R Salazar-Banda ; Marcos R V Lanza ; Cristina Saez ; Manuel A Rodrigo
In this work, it is proposed a novel strategy to increase the photostability of the ZnO photoelectrocatalyst under prolonged light irradiation, without the addition or deposition of metals and/or semiconductor oxides during their synthesis. This strategy is based on the use of a mixed metal oxide (MMO-Ru0.3Ti0.7O2) coating as the substrate for the electrodeposition of ZnO. To assess it, the electrodeposition of ZnO films on Ti and Ti/MMO substrates and the photoelectrocatalytic activity of these materials for the degradation of the herbicide clopyralid were studied. The results showed that the substrate directly influenced the photo-stability of the ZnO film. Under the incidence of UV light and polarization, the novel Ti/MMO/ZnO electrode showed greater photocurrent stability as compared to Ti/ZnO, which is a very important outcome because the behavior of these electrodes was similar when compared in terms of the degradation of clopyralid. Single electrolysis was not able to degrade efficiently clopyralid at the different potentials studied. However, the irradiation of UV light on the polarized surface of the Ti/ZnO and Ti/MMO/ZnO electrodes increased markedly the degradation rate of clopyralid. A synergistic effect was observed between light and electrode polarization, since the rate of degradation of clopyralid was twice as high in photoelectrocatalysis (PhEC) than in photocatalysis (PhC) and different intermediates were formed. From these results, mechanisms of degradation of clopyralid for the PhC and PhEC systems with the Ti/ZnO and Ti/MMO/ZnO electrodes were presented. Therefore, the Ti/MMO/ZnO electrode could be a cheap and simple alternative to be applied in the efficient photodegradation of organic pollutants, presenting the great advantage of having a facile synthesis and high capacity to work at relatively low potentials.
1998-07-01·Toxicology and Applied Pharmacology3区 · 医学
S-[(1 and 2)-phenyl-2-hydroxyethyl]cysteine-induced alterations in renal mitochondrial function in male Fischer-344 rats
3区 · 医学
作者: Chakrabarti, Saroj K. ; Denniel, Claude ; Malick, M. Anwar ; Bai, Chengjiang
Previous studies from our laboratory have shown that mitochondrial dysfunction may be an important early event in S-[(1 and 2)-phenyl-2-hydroxyethyl]cysteine (PHEC)-induced cytotoxicity in isolated rat renal proximal tubules. The present study has therefore examined in more detail PHEC-induced mitochondrial dysfunction, both in vivo and in vitro, using isolated renal cortical mitochondria. Renal cortical mitochondria isolated from PHEC-treated rats in vivo showed depressed effects on the mitochondrial respiration and oxidative phosphorylation in both a dose (0, 250, and 500 micromol/kg iv)- and time (0-24 h)-dependent manner in the presence of both succinate (Site 2) and malate plus alpha-ketoglutarate (Site 1) as respiratory substrates, with initial significant depression occurring as early as 4 h following treatment with 500 micromol PHEC/kg. Similar mitochondrial dysfunctions were observed in vitro in concentration- and time-dependent manners with both respiratory substrates. PHEC also caused a marked dose-dependent inhibition of mitochondrial succinate dehydrogenase and NADH cytochrome c reductase activities both in vivo and in vitro, with initial inhibition occurring as early as 4 h after in vivo administration and 45 min after exposure to PHEC in vitro, while the NADH dehydrogenase activity was not considerably inhibited. The mitochondrial ATPase activity was significantly decreased 4 and 24 h following treatment with PHEC (500 micromol/kg). These results suggest that PHEC exerts its inhibitory effect on the mitochondrial respiration and oxidative phosphorylation through the action on the mitochondrial electron transport chain. PHEC significantly reduced the activity of adenine nucleotide translocase as well as the net uptake of substrates by mitochondria without affecting their efflux within 2-4 h after its injection (500 micromol/kg). On the other hand, significant renal damage, as assessed by morphological study, appeared as early as 24 h following such treatment. The observation of similar effects after both in vivo and in vitro exposures may suggest that the effect on mitochondria may have a pathogenic role in PHEC-induced renal injury in rats. PHEC produces mitochondrial toxicity that results from an inactivation of mitochondrial anionic substrate transporters as well as from an inhibition of activities of adenine nucleotide translocase and dehydrogenases.
1996-04-01·Toxicology and Applied Pharmacology3区 · 医学
S-[(1 and 2)-Phenyl-2-hydroxyethyl]cysteine-induced cytotoxicity to rat renal proximal tubules
3区 · 医学
作者: Chakrabarti, Saroj K. ; Denniel, Claudie
S-[(1 and 2)-phenyl-2-hydroxyethyl]-glutathione is nephrotoxic in rats through its metabolic conversion to corresponding cysteine-S-conjugate, e.g., S-[(1 and 2)-phenyl-2-hydroxyethyl]-cysteine (PHEC). The present study was carried out to determine the mechanism of PHEC-induced toxicity in isolated rat renal proximal tubules. PHEC decreased tubule viability in concentration (0-2 mM)- and time (0-3 hr)-dependent manner, with initial decreases occurring 2 hr after exposure. Tubule basal and nystatin-stimulated oxygen consumption decreased before cell death following exposure to 0.5 and 1 mM PHEC. Assessment of direct mitochondrial function within the proximal tubules showed that respiration was reduced in the absence and presence of a phosphate acceptor using site II (succinate) and site I (malate/glutamate) respiratory substrates 30 and 45 min after exposure to 0.5 and 1 mM PHEC. Exposure of proximal tubules to 1 mM PHEC caused a time-dependent decline of mitochondrial membrane potential (as measured by the uptake of the cationic fluorescent dye, rhodamine 123 by the proximal tubules) and depletion of ATP content with initial decrease occurring as early as 30 min after the exposure. Glutathione depletion and lipid peroxidation occurred within 90 min clearly preceding cell death after exposure to 0.5 and 1 mM PHEC. Pretreatment with 1 mM deferoxamine prevented PHEC-induced lipid peroxidation but did not prevent PHEC-induced cytotoxicity, whereas deferoxamine pretreatment prevented lipid peroxidation, mitochondrial dysfunction, and cytotoxicity after exposure to 0.5 mM tertiary-butyl hydroperoxide, suggesting that iron-mediated lipid peroxidation does not contribute to PHEC-induced proximal tubule cell death. Pretreatment of renal proximal tubules with 10 mM fructose failed to prevent the change in mitochondrial membrane potential, the ATP depletion and cytotoxicity caused by 1 mM PHEC, indicating that the glycolytic pathway is not important in renal proximal tubule respiration and cell injury. Pretreatment of renal tubules with aminooxyacetic acid failed to prevent the mitochondrial dysfunction induced by 1 mM PHEC, indicating an absence of further metabolism of PHEC by a beta-lyase-dependent pathway. It is therefore proposed that the alteration of mitochondrial functions and the consequent loss of cellular energy supplies can represent the mechanisms by which PHEC expressed its acute cytotoxicity.