Microbial niches and dynamics of antibiotic resistance genes in a bio-enhanced granular-activated carbon biofilm treating greywater.

Accumulation and transmission of antibiotic resistance genes (ARGs) in greywater treatment systems present risks for its reuse. In this study, a gravity flow self-supplying oxygen (O2) bio-enhanced granular activated carbon dynamic biofilm reactor (BhGAC-DBfR) was developed to treat greywater. Maximum removal efficiencies were achieved at saturated/unsaturated ratios (RSt/Ust) of 1:1.1 for chemical oxygen demand (97.6 ± 1.5%), linear alkylbenzene sulfonates (LAS) (99.2 ± 0.5%), NH4+-N (99.3 ± 0.7%) and total nitrogen (85.3 ± 3.2%). Microbial communities were significantly different at various RSt/Ust and reactor positions (P < 0.05). The unsaturated zone with low RSt/Ust showed more abundant microorganisms than the saturated zone with high RSt/Ust. The reactor-top community was predominant by aerobic nitrification (Nitrospira) and LAS biodegradation (Pseudomonas, Rhodobacter and Hydrogenophaga) related genera; but reactor-bottom community was predominant by anaerobic denitrification and organics removal related genera (Dechloromonas and Desulfovibrio). Most of the ARGs (e.g., intI-1, sul1, sul2 and korB) were accumulated in the biofilm, which were closely associated with microbial communities at reactor top and stratification. The saturated zone can achieve over 80% removal of the tested ARGs at all operation Phases. Results suggested that BhGAC-DBfR can provide assistance in blocking the environment dissemination of ARGs during greywater treatment.

Slowly Repaired Bulky DNA Damages Modulate Cellular Redox Environment Leading to Premature Senescence.

Treatments on neoplastic diseases and cancer using genotoxic drugs often cause long-term health problems related to premature aging. The underlying mechanism is poorly understood. Based on the study of a long-lasting senescence-like growth arrest (10-12 weeks) of human dermal fibroblasts induced by psoralen plus UVA (PUVA) treatment, we here revealed that slowly repaired bulky DNA damages can serve as a "molecular scar" leading to reduced cell proliferation through persistent endogenous production of reactive oxygen species (ROS) that caused accelerated telomere erosion. The elevated levels of ROS were the results of mitochondrial dysfunction and the activation of NADPH oxidase (NOX). A combined inhibition of DNA-PK and PARP1 could suppress the level of ROS. Together with a reduced expression level of BRCA1 as well as the upregulation of PP2A and 53BP1, these data suggest that the NHEJ repair of DNA double-strand breaks may be the initial trigger of metabolic changes leading to ROS production. Further study showed that stimulation of the pentose phosphate pathway played an important role for NOX activation, and ROS could be efficiently suppressed by modulating the NADP/NADPH ratio. Interestingly, feeding cells with ribose-5-phosphate, a precursor for nucleotide biosynthesis that produced through the PPP, could evidently suppress the ROS level and prevent the cell enlargement related to mitochondrial biogenesis. Taken together, these results revealed an important signaling pathway between DNA damage repair and the cell metabolism, which contributed to the premature aging effects of PUVA, and may be generally applicable for a large category of chemotherapeutic reagents including many cancer drugs.