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Background: The black soldier fly (Hermetia illucens) is gaining attention as an efficient decomposer of food waste. However, recalcitrant compounds such as plastics mixed into food waste may have negative effects on its growth and survival. Moreover, its efficiency of food waste degradation may also be affected by plastics. In addition, salt (NaCl) can also be present in high concentrations, which also reduces the efficiency of H. illucens-mediated food waste treatment. In this study, we assessed the growth of black soldier fly larvae (BSFL) reared on food waste containing polyethylene (PE) and polystyrene (PS) and NaCl. The weight of BSFL was measured every 2-4 days. Survival and substrate reduction rates and pupation ratio were determined at the end of the experiment. Results: The total larval weight of Hermetia illucens reared on food waste containing PS was greater than that of the control on days 20 and 24. However, the survival rate was lower in the group treated with 5% PS, as was substrate reduction in all PS-treated groups. The weight of BSFL reared on food waste containing PE was lower than that of the control on day 6. PE in food waste did not affect the survival rate, but the pupation ratio increased and substrate consumption decreased with increasing PE concentrations. Regardless of the plastic type, the addition of NaCl resulted in decreased larval weight and pupation ratio. Conclusions: Larval growth of black soldier fly was inhibited not by plastics but by substrate salinity. Additional safety assessments of larvae reared on food waste containing impurities are needed to enable wider application of BSFL in vermicomposting.

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MDC1 is critical component of the DNA damage response (DDR) machinery and orchestrates the ensuring assembly of the DDR protein at the DNA damage sites, and therefore loss of MDC1 results in genomic instability and tumorigenicity. However, the molecular mechanisms controlling MDC1 expression are currently unknown. Here, we show that miR-22 inhibits MDC1 translation via direct binding to its 3 0 untranslated region, leading to impaired DNA damage repair and genomic instability. We demonstrated that activated Akt1 and senescence hinder DDR function of MDC1 by upregulating endogenous miR-22. After overexpression of constitutively active Akt1, homologous recombination was inhibited by miR-22-mediated MDC1 repression. In addition, during replicative senescence and stress-induced premature senescence, MDC1 was downregulated by upregulating miR-22 and thereby accumulating DNA damage. Our results demonstrate a central role of miR-22 in the physiologic regulation of MDC1-dependent DDR and suggest a molecular mechanism for how aberrant Akt1 activation and senescence lead to increased genomic instability, fostering an environment that promotes tumorigenesis. Cancer Res; 75(7); 1298-310. Ó2015 AACR.