The possibility that NO might be endogenously produced and, therefore, play specific roles in response to heavy metals has been poorly investigated

The possibility that NO might be endogenously produced and, therefore, play specific roles in response to heavy metals has been poorly investigated. Cd2+ toxicity by favoring Cd2+ versus Ca2+ uptake and by initiating a cellular pathway resembling those activated upon iron deprivation. Nitric oxide (NO) is usually a hydrophobic gaseous molecule and a diffusible free radical. In animal cells, NO is usually catalyzed from l-Arg by the heme-containing enzymes nitric oxide synthases (NOS). It serves as a signaling molecule and, when produced by the immune system, functions as a cytotoxic agent against invading pathogens or tumor cells (Schmidt and Walter, 1994). The pleiotropic effects of NO in biological systems are related to its ability to react with molecular oxygen, superoxide anion, metal cations, and thiols. In particular, NO modulates the activity of a broad range of proteins by binding to crucial Cys residues and to heme or iron-sulfur centers (Stamler et al., 1992). Depending on its surrounding microenvironment, notably the presence of other free radicals, the activity and localization of NOS isoforms, and its overall level, NO was shown to exhibit antioxidant or prooxidant effects (Melino et al., 2000). BMS-193885 When produced at higher concentrations under pathophysiological contexts, NO is usually believed to display prooxidant effects and to promote cytotoxic actions contributing, for instance, to neurodegeneration BMS-193885 or inflammation (Radi, 2004). Almost a decade has passed since the realization of the importance of NO in herb biology (Delledonne et al., 1998; Durner et al., 1998). NO was shown to participate in a wide spectrum of physiological processes, including germination, root growth, gravitropic bending, control of the timing of flowering, stomatal closure, and growth regulation of pollen tubes (Wilson et al., 2007; Besson-Bard et al., 2008b). Furthermore, NO has also been implicated in the herb adaptive response to biotic and abiotic stresses, notably by acting as a signaling molecule (Gould et al., 2003; Delledonne, 2005). It is becoming apparent that NO mediates its effects through roots to aluminum led to an inhibition of NOS activity and consequently of NO production in root apical cells (Tian et al., 2007). Similarly, NO production in the transition zone of Arabidopsis (and genes encoding a ferric chelate reductase and a ferrous iron transporter, respectively, that function together for iron uptake from your ground (Ling et al., 2002). Therefore, depending on iron availability, herb cells use NO as an intracellular transmission to promote iron sequestration or BMS-193885 uptake, highlighting a central function for NO in the control of iron homeostasis. Cadmium (Cd2+) is a heavy metal displaying harmful effects in plants. It is taken up by roots and can be translocated into aerial organs, where it preferentially accumulates in trichomes around the leaf surface (Salt et al., 1995). Cd2+ pollution is usually of major concern, since it hampers herb growth by triggering inhibition of photosynthesis and nitrogen metabolism and by decreasing water and mineral nutrient uptake. Moreover, Cd2+ accumulation in crops compromises their commercial value and Mouse monoclonal to P504S. AMACR has been recently described as prostate cancerspecific gene that encodes a protein involved in the betaoxidation of branched chain fatty acids. Expression of AMARC protein is found in prostatic adenocarcinoma but not in benign prostatic tissue. It stains premalignant lesions of prostate:highgrade prostatic intraepithelial neoplasia ,PIN) and atypical adenomatous hyperplasia. presents a potential risk to human health. The possibility that herb exposure to Cd2+ might modulate NO production has been reported, but conflicting results have been published regarding the impact of Cd2+ on NO production. Depending on the biological model, either Cd2+-mediated induction (Bartha et al., 2005; Kopyra et al., 2006) or inhibition (Rodrguez-Serrano et al., 2006) of NO production has been reported. In the corresponding studies, treatment of plants with artificially generated NO was shown to protect herb tissues against the oxidative damage triggered by Cd2+ by promoting the scavenging of reactive oxygen species (ROS) directly through chemical processes or indirectly via the activation of ROS-scavenging enzymes (Kopyra et al., 2006; Noriega et al., 2007). Although useful, these studies did not take into account the possibility that NO might be endogenously produced in response to Cd2+ and, therefore, might exert specific roles in this particular physiological.