No abstract

Lignin, an abundant plant biopolymer, is known to possess antioxidant and UV protectant properties in its native state. Nanoparticles exhibit either improved or different properties corresponding to their bulk materials or parent polymers. In the present study, using nanoprecipitation method, dioxane lignin nanoparticles (DLNP) and alkali lignin nanoparticles (ALNP) are fabricated from two different sources of lignin, i.e., hardwood dioxane lignin (DL) extracted from subabul stems and softwood alkali lignin (AL) which is available as a commercial source. Both DLNP and ALNP were fabricated in spherical shape with mean size of 80À104 nm. Analysis of radical scavenging activity revealed that both DLNP and ALNP possess higher antioxidant activity when compared with their parent polymers DL and AL, respectively. UV protectant potential of DLNP and ALNP was validated by monitoring the survival rates of Escherichia coli upon UVinduced mortality. DLNP and ALNP were more efficient than DL and AL in protecting E. coli against UV-irradiation-induced mortality. However, upon irradiation for different time periods, DLNP offered pronounced protection for E. coli against UV when compared with ALNP. Thus, the present study demonstrates that the antioxidant and UV protection properties of DLNP can be exploited further in food, pharmaceutical and cosmetic industries.

Plant respiration is characterized by two pathways for electron transfer to O(2), namely the cytochrome pathway (CP) that is linked to ATP production, and the alternative pathway (AP), where electrons from ubiquinol are directly transferred to O(2) via an alternative oxidase (AOX) without concomitant ATP production. This latter pathway is well suited to dispose of excess electrons in the light, leading to optimized photosynthetic performance. We have characterized T-DNA-insertion mutant lines of Arabidopsis thaliana that do not express the major isoform, AOX1A. In standard growth conditions, these plants did not show any phenotype, but restriction of electron flow through CP by antimycin A, which induces AOX1A expression in the wild-type, led to an increased expression of AOX1D in leaves of the aox1a-knockout mutant. Despite the increased presence of the AOX1D isoform in the mutant, antimycin A caused inhibition of photosynthesis, increased ROS, and ultimately resulted in amplified membrane leakage and necrosis when compared to the wild-type, which was only marginally affected by the inhibitor. It thus appears that AOX1D was unable to fully compensate for the loss of AOX1A when electron flow via the CP is restricted. A combination of inhibition studies, coupled to metabolite profiling and targeted expression analysis of the P-protein of glycine decarboxylase complex (GDC), suggests that the aox1a mutants attempt to increase their capacity for photorespiration. However, given their deficiency, it is intriguing that increase in expression neither of AOX1D nor of GDC could fully compensate for the lack of AOX1A to optimize photosynthesis when treated with antimycin A. We suggest that the aox1a mutants can further be used to substantiate the current models concerning the influence of mitochondrial redox on photosynthetic performance and gene expression.

These results suggest that AOX1A plays a significant role in sustaining the chloroplastic redox state and energization to optimize photosynthesis by regulating cellular redox homeostasis and ROS generation when electron transport through the COX pathway is disturbed at complex III.