Pb exposure causes non-linear accumulation of Pb in D. melanogaster controlled by metallothionein B and exerts ecological effects.

Pb pollution can harm human health and the ecosystem. Therefore, it is worthwhile to study the metabolic processes of heavy metals in individual bodies and their influence on ecological systems. In this work, we analyzed the genetic responses and physiological changes of D. melanogaster which took diets exposed to different doses of Pb using transcriptomic analysis, ICP-MS, and various other physiological methods. We found that the Pb accumulated in D. melanogaster in a nonlinear pattern with the increase of Pb content in food. Metallothioneins (Mtns), especially the MtnB directly affects the accumulation and excretion of metal Pb in D. melanogaster, and causes the nonlinear accumulation. Metal regulatory transcription factor-1 (MTF-1) is involved in the regulation of Pb-induced high expressions of Mtns. Furthermore, an interaction between the metal metabolism pathway and xenobiotic response pathway leads to the cross-tolerances of Pb-exposed D. melanogaster to insecticides and other toxins. The oxidative stress induced by Pb toxicity may be the bridge between them. Our findings provide a physiological and molecular genetic basis for further study of the accumulation and metabolism of Pb in D. melanogaster.

Xenobiotic responses of Drosophila melanogaster to insecticides with different modes of action and entry.

Depending on their chemical structure, insecticides enter the insect body either through the cuticle or by ingestion (mode of entry [MoE]), and, naturally, harm or even kill insects through different mechanisms (modes of action). In parallel, they trigger a systemic detoxification response, especially by activation of detoxification gene expression. We monitored the acute genetic alterations of known xenobiotic response target genes against five different insecticides with two most common MoEs (contact toxicity and stomach toxicity), found that: 1. only a few genes were detected responding to acute exposure to insecticides (LD90 ); 2. The expression of cyp12d1 was upregulated in all experiments, except for dichlorodiphenyltrichloroethane exposure, suggesting that cyp12d1 is a general first response gene of the xenobiotic response; 3. The contact and stomach entries did not show any notable difference, both MoEs induced the response of JNK signaling pathway, possibly serving as the driver of the response of cyp12d1 and a few other genes. In conclusion, the changes in gene expression levels were relatively modest and no significant differences were found between the two MoEs, so the insecticide entry route does not seem to have an impact on the detoxification response. However, the two MoEs of the same insecticide showed different efficiencies in our test. Thus, the study of these two MoEs will help to develop more efficient release and management methods for the use of such insecticides.