JNK- and Rel-Mediated Regulation of Inflammation and Neurotoxicity in Nauphoeta Cinerea Exposed to Methylmercury and Monosodium Glutamate

Food contaminants are closely monitored to establish food safety profiles. Previously, we used the lobster cockroach to delineate the oxidative and antioxidant activities that characterize exposure to the organometallic cation (methylmercury; MeHg) sometimes found in fish and the common cooking seasoning (NaCl and MSG). Here, we further examined the mechanism of inflammatory response to MeHg, NaCl, and MSG, in an attempt to establish the crosstalk between redox and inflammatory signaling during heavy metal exposure in food. The insects were exposed to diets contaminated with MeHg, NaCl, and MSG for 21 days. Subsequently, mRNA from head homogenate was used to quantify the expression of a member of the Nox/Duox NADPH oxidases that produce reactive oxygen species (DUOX), as well as target genes of the JNK, TOLL, and UPD3/JAK/STAT pathways. MeHg exposure deregulated redox and inflammation-related genes, including upregulated DUOX in the MeHg group, upregulated Reaper, UPD3, and SOCS36E in the MeHg + NaCl group, and downregulated Reaper in the MeHg + MSG group. Both MeHg + NaCl and MeHg + MSG exposures upregulated PVF, EGR, and REL and downregulated FOXO levels. Our results suggest a role for the activation of the Nox/Duox NADPH oxidases, alongside JNK and Rel signaling during MeHg and MSG exposure, therefore offering insights for handling heavy metal poisoning and showcasing Nauphoeta cinerea as a viable model for understanding redox and inflammatory signaling.