Aluminum Disrupts Motor Function, Cholinergic System, Redox Balance, Pro-Apoptotic and Pro-Inflammatory Pathways in Nauphoeta cinerea Model.

This study sought to investigate the utility of the lobster cockroach (Nauphoeta cinerea) to understand the effect of aluminum (Al) exposure on neural tissues. We randomly divided lobster cockroach nymphs into three groups: control, 125 mg/g AlCl₁, and 250 mg/g AlCl₁. The cockroaches were maintained on an Al-containing dietary regimen for 3, 7 and 14 days and subsequently assessed for neurolocomotor indices. Cockroach heads were then dissected on ice and the neural tissues were isolated to assay cell viability, acetylcholinesterase, monoamine oxidase, glutathione-S-transferase, total thiol and total reactive oxygen and nitrogen species (RONS). In addition, mRNA levels of antioxidant, PI3K/AKT pro-apoptotic and JNK/UPD3 pro-inflammatory pathway genes were analyzed on day 14. Locomotor indices were reduced during these exposure periods, but there was no significant difference in the survival rate of the cockroaches. The biochemical analysis revealed a significant increase in AChE activity in Al-exposed cockroaches across the three points of analysis, while cell viability and mRNA levels of superoxide dismutase, catalase and thioredoxin were significantly reduced by day 14. Furthermore, significant increases in total RONS, total thiol, GST activity, and mRNA levels of GST, DUOX, Akt, Egr, Pvf and upd3 were observed in Al-exposed groups. Al-induced impairments were largely dose- and time-dependent. Collectively, we demonstrated, for the first time, the utility of Nauphoeta cinerea to delineate the mechanisms of Al-induced neurotoxicity and neurodegeneration. The behavioral deficits were accompanied by increased AChE activity and ROS production, impairment of the antioxidant system, and modulation of the PI3K/Akt and JNK/upd3 signaling pathways that modulate apoptosis and inflammatory signals, respectively.