Influence of nitrogen form on the phytoextraction of cadmium by a newly discovered hyperaccumulator Carpobrotus rossii

Using hyperaccumulator plants is an important method to remove heavy metals from contaminated land. Carpobrotus rossii, a newly found Cd hyperaccumulator, has shown potential to remediate Cd-contaminated soils. This study examined the effect of nitrogen forms on Cd phytoextraction by C. rossii. The plants were grown for 78 days in an acid soil spiked with 20 mg Cd kg(-1) and supplied with (NH4)(2)SO4, Ca(NO3)(2), urea, and chicken manure as nitrogen (N) fertilizers. Nitrification inhibitor dicyandiamide (DCD) was applied to maintain the ammonium (NH4+) form. Nitrogen fertilization increased shoot biomass but decreased root biomass with the highest shoot biomass occurring in the manure treatment. Compared to the no-N control, urea application did not affect shoot Cd concentration, but increased Cd content by 17 % due to shoot biomass increase. Chicken manure significantly decreased CaCl2-extractable Cd in soil, and the Cd concentration and total Cd uptake in the plant. Rhizosphere pH was the highest in the manure treatment and the lowest in the NH4+ treatments. The manure and nitrate (NO3-) treatments tended to have higher rhizosphere pH than their respective bulk soil pH, whereas the opposite was observed for urea and NH4+ treatments. Furthermore, the concentrations of extractable Cd in soil and Cd in the plant correlated negatively with rhizosphere pH. The study concludes that urea significantly enhanced the Cd phytoaccumulation by C. rossii while chicken manure decreased Cd availability in soil and thus the phytoextraction efficiency

Palmitic acid in chicken granulosa cell death-lipotoxic mechanisms mediate reproductive inefficacy of breeder hens

In vivo and in vitro approaches were used to elucidate mechanisms of palmitate-induced cytotoxicity of follicle granulosa cells in fuel-overloaded broiler hens. In contrast to their energy-restricted counterparts, broiler breeder hens fed ad libitum for 2 wk had dyslipidemia, atresia within hierarchical ovarian follicles, and a 34% reduction in egg production (P 0.05). Based on vital staining of freshly isolated granulosa cells with annexin V/propidium iodide, there were increases in apoptosis consistent with suppressed Akt activation (P 0.05). Supplementing primary granulosa cell cultures with 0.5 mM palmitate for 48 or 96 h increased apoptosis (P 0.05). Palmitate-induced cell death was accompanied by increased acyl-CoA oxidase, carnitine palmitoyl transferase-1, serine palmitoyl transferase, and sphingomyelinase transcripts and increased concentrations of proinflammatory interleukin-1 (P 0.05). Triacsin-C inhibition of fatty acyl-CoA synthesis blunted interleukin-1 production and rescued granulosa cultures from palmitate-induced cell death. That there was partial to complete prevention of cell death with addition of the free radical scavenger pyrrolidine dithiocarbamate, the sphingomyelinase inhibitor imipramine, or the de novo ceramide synthesis inhibitor fumonisin B1, supported the notion that palmitate-induced granulosa cell cytotoxicity operated through a palmitate-derived metabolite. Palmitoyl-CoA may be channeled into -oxidation and/or into bioactive metabolites that increase free radical generation, an inflammatory response, and ceramide production. In conclusion, palmitate-derived metabolites activated apoptotic machinery in avian granulosa cells, which caused ovarian follicular atresia and reduced egg production in fuel-overloaded broiler breeder hens