Microbial community associated with hydrogen production and volatile fatty acids (VFAs) accumulation was characterized in acidogenic hydrogenesis using molasses wastewater as a feedstock. Hydrogen and VFAs production were measured under an organic loading rate (OLR) from 19 to 35 g‐COD l−1 day−1. The active microbial community was analysed using RNA‐based massively parallel sequencing technique, and their correlation patterns were analysed using networking analysis. The continuous stirred tank reactor achieved stable hydrogen production at different OLR conditions, and the maximum hydrogen production rate (HPR) was 1·02 L‐H2 l−1 day−1 at 31·0 g‐COD l−1 day−1. Butyrate (50%) and acetate (38%) positively increased with increase in OLR. Total VFA production stayed around 7135 mg l−1 during the operation period. Although Clostridiales and Lactobacillales were relatively abundant, the HPR was positively associated with Pseudomonadaceae and Micrococcineae. Total VFA and acetate, butyrate and propionate concentrations were positively correlated with lactic acid bacteria (LAB) such as Bacillales, Sporolactobacillus and Lactobacillus. The close relationship between Pseudomonadaceae and Micrococcineae, and LAB play important roles for stable hydrogen and VFA production from molasses wastewater. Microbial information on hydrogen and VFA production can be useful to design and operate for acidogenic hydrogenesis using high strength molasses wastewater.
Mitochondrial dysfunction is implicated in age-related degenerative disorders such as Alzheimer's disease (AD). Maintenance of mitochondrial dynamics is essential for regulating mitochondrial function. Aβ oligomers (AβOs), the typical cause of AD, lead to mitochondrial dysfunction and neuronal loss. AβOs have been shown to induce mitochondrial fragmentation, and their inhibition suppresses mitochondrial dysfunction and neuronal cell death. Oxidative stress is one of the earliest hallmarks of AD. Cyclin-dependent kinase 5 (Cdk5) may cause oxidative stress by disrupting the antioxidant system, including Prx2. Cdk5 is also regarded as a modulator of mitochondrial fission; however, a precise mechanistic link between Cdk5 and mitochondrial dynamics is lacking. We estimated mitochondrial morphology and alterations in mitochondrial morphology-related proteins in Neuro-2a (N2a) cells stably expressing the Swedish mutation of amyloid precursor protein (APP), which is known to increase AβO production. We demonstrated that mitochondrial fragmentation by AβOs accompanies reduced mitofusin 1 and 2 (Mfn1/2) levels. Interestingly, the Cdk5 pathway, including phosphorylation of the Prx2-related oxidative stress, has been shown to regulate Mfn1 and Mfn2 levels. Furthermore, Mfn2, but not Mfn1, over-expression significantly inhibits the AβO-mediated cell death pathway. Therefore, these results indicate that AβO-mediated oxidative stress triggers mitochondrial fragmentation via decreased Mfn2 expression by activating Cdk5-induced Prx2 phosphorylation. Mitochondrial fragmentation induced by amyloid-beta oligomer (AβOs) which is generated from the Swedish mutation of amyloid precursor protein (APP) accompanies reduced Mfn1/2 levels. Interestingly, the Cdk5 pathway, including phosphorylation of the Prx2-related oxidative stress, has been shown to regulate Mfn1/2. Furthermore, Mfn2 over-expression significantly inhibits the AβO-mediated neuronal cells death pathway, but not Mfn1 over-expression. Therefore, these results indicate that AβO-mediated oxidative stress triggers mitochondrial fragmentation via decreased Mfn2 expression by activating Cdk5-induced Prx2 phosphorylation. ATP, adenosine triphosphate; Bax, Bcl-2-associated X protein; Bcl-2, B-cell lymphoma 2; Cdk5, Cyclin-dependent kinase; Cyt C, cytochrome C; Mfn2, mitofusin 2; Prx2, peroxiredoxin 2; ROS, reactive oxygen species.
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