crystallinum and A. thaliana must be Ganetespib STA-9090 related to the degree of resistance to salinity in each plant species, and thus the increase of the NADP-ICDH activity must be related to the NADPH requirement in each organ. Thus, in the case of M. crystallinum under salt stress the excess Na+ is transported very efficiently to the leaves whereas only a minor part is accumulated in root tissue [46]; however, in Arabidopsis the situations is totally different, considering the sensitivity of this plant to salinity in comparison to M. crystallinum [2].In summary, these data suggest that the activities of the NADPH-generating dehydrogenases, especially the NADP-ICDH in roots, contributed to maintaining the cellular redox status as a mechanism to support the antioxidative system during the nitro-oxidative stress generated by salinity stress in Arabidopsis.
Thus, it is proposed that NADP-ICDH dehydrogenase acts in Arabidopsis seedlings as a second barrier in the response mechanism of salinity stress, but they could also have a protective function in other types of abiotic stress.AcknowledgmentsThis work was supported by ERDF-cofinanced grants from the Ministry of Science and Innovation (BIO2009-12003-C02-01 and BIO2009-12003-C02-02), Spain. Confocal laser scanning microscopy analyses were carried out at the Technical Services of the University of Ja��n. It is also acknowledged the excellent technical support provided by Mr. Carmelo Ru��z-Torres.
Serratia marcescens is an opportunistic pathogen, increasingly recognized as a cause of morbidity in nosocomial settings.
They are becoming an increasingly important cause of many outbreaks in neonatal intensive care units [1, 2]. The bacteria are frequent agents of catherization-associated infections. They are an etiological agent of wounds, urinary, and respiratory tract infections, keratitis, arthritis, meningitis, endocarditis, osteomyelitis, and septicemia [2].Although there are frequent reports of nosocomial Serratia spp. outbreaks, the possible mechanism of their pathogenicity is still poorly understood and probably is complex and multifactorial. The strains secrete a number of toxins and exoenzymes: proteases, chitinases, a lipase, and nucleases, which may directly contribute to cellular cytotoxicity [2]. Some strains produce pore-forming toxins that represent hemolysin ShlA and ShlB.
One of the most potent virulence factors of Serratia spp. is ShlA which causes hemolysis of human erythrocytes and the release of the inflammatory Drug_discovery mediators from leucocytes. The toxin was shown to exhibit a cell-bound cytotoxicity [3]. Carbonell at al. [4] reported that S. marcescens strains produce an extracellular toxin that revealed cytotoxic activity to human epithelial cells. The toxin did not cause hemolysis of human erythrocytes.