Sodium inhibition of fermentative hydrogen production

摘要

A continuous-stirred-tank reactor (CSTR) was fed with low-sodium influent containing 0.27 g of Na~+/L for 70 days (Phase I), and then subjected to higher concentrations of Na~+/L, i.e. 2.41 (Phase Ⅱ), 5.36 (Phase Ⅲ), and 10.14 g (Phase Ⅳ-1). At the quasi-steady state of each phase, biomass was sampled for an acute sodium toxicity assay. Unlike the control biomass, which exhibited a monotonic decrease of specific H_2 production activity (SHPA) with increasing sodium concentration from 0.27 to 21.00 g Na~+/L, the acclimated biomass maintained their activity up to 6.00 g Na~+/L. Soluble microbial product analysis revealed that a sudden increase of the exterior sodium concentration changed the metabolic pathway such that it became favorable to lactate production while depressing butyrate production. Meanwhile, when the biomass was allowed for sufficient time to adapt to the chronic toxicity condition, the volumetric H_2 production rate (VHPR) was maintained above 4.05 L H_2/L/d at up to Phase Ⅲ. However, an irrecoverable H_2 production drop was observed at Phase Ⅳ-1 with a significant increase of lactate and propionate production. Although the sodium concentration decreased to 8.12 (Phase Ⅳ-2), 6.61 (Phase Ⅳ-3), and 5.36 g Na~+/L (Phase Ⅴ) at further operation, the performance was never recovered. A PCR-DGGE analysis revealed that lactic acid bacteria (LAB) and propionic acid bacteria (PAB) were only detected at Phases Ⅳ and Ⅴ, which are not capable of producing H_2.