RESUMEN
This study used a porcine model to systematically investigate whether carboxyfullerene C60(CF-C60) can be used for sperm preservation. The results indicated that CF-C60 supplementation can preserve porcine sperm quality during storage at 17 °C. This effect was attributable to an improvement in the antioxidant capacity of sperm through a decrease in the reactive oxygen species (ROS) level. Additionally, CF-C60 can maintain mitochondrial function, inhibit sperm apoptosis through the ROS/Cytochrome C (Cyt C)/Caspase 3 signaling pathway, and mediate suppression of bacterial growth through the effects of ROS. Finally, the results of artificial insemination experiments indicated that insemination with CF-C60-treated sperm can increase the total number of offspring born and reduce the number of deformed piglets. Thus, CF-C60 is safe for use as a component of semen diluent for sperm storage.
The development of novel porcine sperm protective agents holds profound significance for improving fertility quality and promoting reproductive health. Excessive oxidative stress and bacterial contamination, leading to sperm apoptosis, are the 2 major factors affecting the decline of porcine sperm quality. Recently, CF-C60 has gained attention as an important nanocarbon derivative with strong antioxidant and antibacterial activity. However, the role and mechanism of CF-C60 in the preservation of mammalian sperm remain unknown. This study aimed to explore the important protective role of CF-C60 in porcine sperm.
Asunto(s)
Antioxidantes , Apoptosis , Fulerenos , Especies Reactivas de Oxígeno , Preservación de Semen , Espermatozoides , Animales , Masculino , Espermatozoides/efectos de los fármacos , Espermatozoides/fisiología , Apoptosis/efectos de los fármacos , Porcinos , Antioxidantes/farmacología , Fulerenos/farmacología , Fulerenos/química , Preservación de Semen/veterinaria , Especies Reactivas de Oxígeno/metabolismo , Inseminación Artificial/veterinariaRESUMEN
To date, metallization studies have been performed with the nanometer-scale template, Tobacco Mosaic Virus (TMV). Here we show that fullerenes as well can be deposited on TMV coat protein in a controlled manner. Two methods were followed for the coating process. First, underivatized fullerene was dispersed in different solvents to bring the underivatized fullerene and wild-type TMV together. Improved depositions were obtained with the fullerene dicarboxylic derivative synthesized via the Bingel method. The form of the coating was analyzed by transmission electron microscopy. Our results demonstrate that the coating efficiency with the carboxy derivative was much better compared to the underivatized fullerene. The goal of coupling a carbon nanoparticle to a biological molecule, the viral coat of TMV, was achieved with the carboxy derivative of fullerene, resulting in the production of navette-shaped nanorods. The interactions between carboxyfullerenes and TMV were investigated through modeling with computational simulations and Gaussian-based density functional theory (DFT) calculations using the Gaussian09 program package. The theoretical calculations supported the experimental findings. This inexpensive and untroublesome method promises new fullerene hybrid nanomaterials in particular shapes and structures.
Asunto(s)
Fulerenos , Nanopartículas , Nanotubos , Virus del Mosaico del Tabaco , Microscopía Electrónica de Transmisión , Nanotubos/química , NicotianaRESUMEN
Background: Asphyxia is the most common cause of brain damage in newborns. Substantial evidence indicates that leukocyte recruitment in the cerebral vasculature during asphyxia contributes to this damage. We tested the hypothesis that superoxide radical ( O 2 â _ ) promotes an acute post-asphyxial inflammatory response and blood-brain barrier (BBB) breakdown. We investigated the effects of removing O 2 â _ by superoxide dismutase (SOD) or C3, the cell-permeable SOD mimetic, in protecting against asphyxia-related leukocyte recruitment. We also tested the hypothesis that xanthine oxidase activity is one source of this radical. Methods: Anesthetized piglets were tracheostomized, ventilated, and equipped with closed cranial windows for the assessment of post-asphyxial rhodamine 6G-labeled leukocyte-endothelial adherence and microvascular permeability to sodium fluorescein in cortical venules. Asphyxia was induced by discontinuing ventilation. SOD and C3 were administered by cortical superfusion. The xanthine oxidase inhibitor oxypurinol was administered intravenously. Results: Leukocyte-venular adherence significantly increased during the initial 2 h of post-asphyxial reperfusion. BBB permeability was also elevated relative to non-asphyxial controls. Inhibition of O 2 â _ production by oxypurinol, or elimination of O 2 â _ by SOD or C3, significantly reduced rhodamine 6G-labeled leukocyte-endothelial adherence and improved BBB integrity, as measured by sodium fluorescein leak from cerebral microvessels. Conclusion: Using three different strategies to either prevent formation or enhance elimination of O 2 â _ during the post-asphyxial period, we saw both reduced leukocyte adherence and preserved BBB function with treatment. These findings suggest that agents which lower O 2 â _ in brain may be attractive new therapeutic interventions for the protection of the neonatal brain following asphyxia.
RESUMEN
Hemorrhagic shock/resuscitation involves overwhelming reactive oxygen species (ROS) that cause oxidative stress, inflammation, and subsequent tissue injury. We investigated the effects of the potent antioxidant carboxyfullerene (C3) on acute liver injury during hemorrhage shock/resuscitation. C3 infusion reduced the alanine aminotransferase (ALT) activity, methemoglobin content, malondialdehyde content, myeloperoxidase activity and expression levels of tumor necrosis factor -α and interleukin-6; it increased superoxide dismutase activity in the liver. The histologic injury score and apoptotic index were also markedly decreased after C3 treatment compared with the vehicle group. Additionally, C3-treated rats showed a significant decrease in nuclear factor-κB DNA binding capacity, which was preceded by reduced phosphorylation of the nuclear factor κB (NF-κB) p65 subunit in the liver. C3 nanoparticles ameliorate oxidative stress, the inflammatory response, and subsequent acute liver injury after hemorrhagic shock/resuscitation. These protective effects appear to be mediated through the inhibition of the nuclear factor-κB pathway. C3 treatment may be a promising strategy to improve tissue injury in hemorrhagic shock/resuscitation.