ABSTRACT
Chalcogenide Ag10As30S60 thin films are prepared using the thermal evaporation technique from the bulk alloy. Deferential Scanning Calorimetry (DSC) curve reveals two crystallization stages for the bulk. The X-ray examination of the as-prepared and annealed films shows that the sample is crystallized in preferential orientations indicated with peaks corresponding the S8 and ternary AsAg3S3 phases. Transmission spectra show that the as-prepared and annealed films have highly transparent over the visible region. The presence of a sharp absorption edge for all films in the transmission spectra recommends Ag10As30S60 thin films as a good optical filter material. The improvement in transparency upon annealing is due to the enhancement in the crystallinity. The decrease in both optical band gap and refractive index of annealed films after crystallization temperatures is discussed in accordance with the structure changes upon annealing.
Subject(s)
Alloys/chemistry , Arsenic/chemistry , Silver/chemistry , Sulfur/chemistry , Crystallization , Light , Refractometry , Surface Properties , Temperature , X-Ray DiffractionABSTRACT
The present study was aimed to investigate the mechanistic aspect of endosulfan toxicity and its protection by taurine in rat testes. Pre-treatment with taurine (100 mg/kg/day) significantly reversed the decrease in testes weight, and the reduction in sperm count, motility, viability and daily sperm production in endosulfan (5 mg/kg/day)-treated rats. Sperm chromatin integrity and epididymal L-carnitine were markedly decreased by endosulfan treatment. Endosulfan significantly decreased the level of serum testosterone and testicular 3ß-HSD, 17ß-HSD, G6PDH and LDH-X. Sperm Δψm and mitochondrial cytochrome c content were significantly decreased after endosulfan. Testicular caspases-3, -8 and -9 activities were significantly increased but taurine showed significant protection from endosulfan-induced apoptosis. Oxidative stress was induced by endosulfan treatment as evidenced by increased H2O2 level and LPO and decreased the antioxidant enzymes SOD, CAT and GPx activities and GSH content. These alterations were effectively prevented by taurine pre-treatment. In conclusion, endosulfan decreases rat testes weight, and inhibits spermatogenesis and steroidogenesis. It induces oxidative stress and apoptosis by possible mechanisms of both mitochondria and non-mitochondria pathways. These data provide insight into the mode of action of endosulfan-induced toxicity and the beneficial role provided by taurine to counteract endosulfan-induced oxidative stress and apoptosis in rat testis.
Subject(s)
Apoptosis/drug effects , Endosulfan/toxicity , Insecticides/toxicity , Oxidative Stress/drug effects , Taurine/pharmacology , Testis/drug effects , Animals , Caspases/metabolism , Catalase/metabolism , Cytochromes c/metabolism , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Hydroxysteroid Dehydrogenases/metabolism , L-Lactate Dehydrogenase/metabolism , Male , Mitochondria/enzymology , Rats , Rats, Wistar , Superoxide Dismutase/metabolism , Testis/cytology , Testis/enzymology , Testosterone/bloodABSTRACT
TCDD, as an endocrine disruptor, is known to impair testicular functions and fertility. To elucidate the mechanism(s) underlying the testicular effects of TCDD, the potential toxicity of TCDD on Sertoli cells was investigated. Furthermore, the study aims to delineate whether mitochondrial fractions of Sertoli cells are involved in mediating the testicular effects of TCDD. Adult rat Sertoli cells were incubated with (5, 10 or 15nM) of TCDD for 6, 12 or 24h. Cell viability, lactate and LDH leakage into media along with lipid peroxidation, ROS generation, SOD, CAT, GPx, GR, γ-GT and ß-glucuronidase activities, GSH content and Δψ(m) were measured. Superoxide anion production, COX and cardiolipin content were measured in mitochondrial fractions. Cell viability was significantly decreased while lactate and LDH leakage into media were increased. ROS generation along with lipid peroxidation was also increased. SOD, CAT, GPx, GR activities and GSH content were significantly decreased. γ-GT and ß-glucuronidase activities were also decreased. Superoxide anion production was increased while COX activity and cardiolipin content were decreased in mitochondrial fractions. Moreover, the Δψ(m) was significantly decreased as measured in Sertoli cells. In conclusion, TCDD impairs Sertoli cell functions and this effect is, at least in part, attributed to oxidative stress. We have also found that TCDD increases mitochondrial superoxide anion production and decreases Δψ(m), COX activity and mitochondrial cardiolipin content. Our findings suggest that mitochondria may play an important role in ROS production, leading to the TCDD-induced oxidative stress response and resulting toxicological consequences in rat Sertoli cells.
