Biodegradation of chloroxylenol by an aerobic enrichment consortium and a newly identified Rhodococcus strain.

Chloroxylenol is a commonly used antimicrobial agent in antibacterial and disinfection products, which has been detected in various environments, such as wastewater treatment plants, rivers, seawater, and even drinking water, with concentrations ranging from ng/L to mg/L. However, the biodegradation of chloroxylenol received limited attention with only sporadic reports available so far. In this study, an efficient chloroxylenol-degrading consortium, which could degrade 20 mg/L chloroxylenol within two days, was obtained after five months of enrichment. Amplicon sequencing analysis revealed a decrease in the α-diversity (e.g., Shannon index and Inv_Simpson index) of the community during the domestication process. Microbial community dynamics were uncovered, with sequences affiliated to Achromobacter, Pseudomonas, and Rhodococcus identified as the most abundant taxonomic groups. From the consortium, five pure isolates were obtained; however, it was found that only one strain of Rhodococcus could degrade chloroxylenol. Strain Rhodococcus sp. DMU2021 could degrade chloroxylenol efficiently under the conditions of temperature 30-40 °C, and neutral/alkaline conditions. Chloroxylenol was toxic to strain DMU2021 and triggered both enzymatic and non-enzymatic antioxidant systems in response. This study provides novel insights into the biodegradation process of chloroxylenol, as well as valuable bioresources for bioremediation.

HOTAIRM1 knockdown reduces MPP+-induced oxidative stress injury of SH-SY5Y cells by activating the Nrf2/HO-1 pathway.

Objective: Parkinson's disease (PD) is the second most common neurodegenerative disease with complex pathogenesis. Although HOXA transcript antisense RNA myeloid-specific 1 (HOTAIRM1) is upregulated in PD, its exact role in HOTAIRM1 is seldom reported. The purpose of this study is to research the effect of HOTAIRM1 on 1-methyl-4-phenylpyridonium (MPP+)-induced cytotoxicity and oxidative stress in SH-SY5Y cells. Methods: SH-SY5Y cells were treated with MPP+ at various concentrations or time points to induce SH-SY5Y cytotoxicity, so as to determine the optimal MPP+ concentration and time point. HOTAIRM1 expression upon MPP+ treatment was analyzed through qRT-PCR. Next, HOTAIRM1 was downregulated to observe the variance of SH-SY5Y cell viability, apoptosis, oxidative stress-related indexes, and protein levels of the Nrf2/HO-1 pathway. In addition, rescue experiments were carried out to assess the role of Nrf2 silencing in HOTAIRM1 knockdown on MPP+-induced oxidative stress in SH-SY5Y cells. Results: MPP+ treatment-induced cytotoxicity and upregulated HOTAIRM1 expression in SH-SY5Y cells in a dose- and time-dependent manner. Mechanically, HOTAIRM1 knockdown enhanced cell viability, limited apoptosis, and oxidative stress, therefore protecting SH-SY5Y cells from MPP+-induced SH-SY5Y cytotoxicity. On the other hand, HOTAIRM1 knockdown activated the protein levels of Nrf2 and HO-1. Nrf2 silencing could counteract the neuroprotective effect of HOTAIRM1 knockdown on in vitro PD model. Conclusion: Our data demonstrated that HOTAIRM1 knockdown could inhibit apoptosis and oxidative stress and activated the Nrf2/HO-1 pathway, therefore exerting neuroprotective effect on the PD cell model.

Genistein acts as antidepressant agent against chronic mild stress-induced depression model of rats through augmentation of brain-derived neurotrophic factor.

In this study, the antidepression effects of genistein were investigated in rats induced with chronic mild stress. Animals were designated into the following groups: normal control, control, 10 mg, and 100 mg. The dose was given for 45 consecutive days via the oral route. Sucrose preference analysis, forced swim, and open field tests were performed, and serum cortisol and monoamine levels in brain tissue were determined. The mRNA and protein expression of brain-derived neurotrophic factor (BDNF) was also examined. Supplementation with genistein significantly increased the sucrose preference ratio, locomotor activity, and monoamines and decreased serum cortisol levels. The mRNA expression of BDNF in the brain tissue was substantially reduced by 0.73% in control rats. However, supplementation with genistein significantly increased BDNF mRNA expression (by 107% and 229.6% in groups 10 mg and 100 mg, respectively). Similarly, the protein expression of BDNF increased by 82.3% and 141.2% in groups 10 mg and 100 mg, respectively. Taken together, these results suggest that supplementation with genistein may be effective against depression.