Parental treatment with selenium protects Caenorhabditis elegans and their offspring against the reproductive toxicity of mercury.

Mercury (Hg) is one of the major pollutants in the environment, which requires effective countermeasures to manage its risk to both human health and the ecosystem. The antagonistic effect of selenium (Se) against methyl mercury (MeHg) and HgCl2 was evaluated using parent and offspring Caenorhabditis elegans (C. elegans) in this study. Through designated acute exposure of 24 h, our results showed that both MeHg and HgCl2 induced dose-dependent reproductive toxicity, including increased germ cell apoptosis, decrease in the number of oocytes, brood size, and sperm activation. The increased germ cell apoptosis was even higher in F1 and F2 generations, but returned to control level in F3 generation. Pretreatment with Se significantly suppressed the reproductive toxicity caused by Hg in both parental worms and their offspring, but had little influence on Hg accumulation. The protective role of Se was found closely related to the chemical forms of Hg: mtl-1 and mtl-2 genes participated in reducing the toxicity of HgCl2, while the gst-4 gene was involved in the reduced toxicity of MeHg. The formation of Se-Hg complex and the antioxidant function of Se were considered as possible antagonistic mechanisms. Our data indicated that pretreatment with Se could effectively protect C. elegans and their offspring against the reproductive toxicity of Hg in different chemical forms, which provided a reference for the prevention of Hg poisoning and essential information for better understanding the detoxification potential of Se on heavy metals.

Transgenerational reproductive toxicity of 2,4,6-trinitrotoluene (TNT) and its metabolite 4-ADNT in Caenorhabditis elegans.

2,4,6-trinitrotoluene (TNT) as an energetic compound widely used in military applications has aroused great concerns in recent years due to its large-scale contamination in soil and water; however, its toxicity is still largely unknown. In this study, we investigated the reproductive toxicity and the transgenerational effects of TNT on Caenorhabditis elegans (C. elegans). Our data showed that exposure to TNT at concentrations ranging from 10 to 100 ng/mL resulted in decreasing the lifespan, brood size, number of oocytes and eggs in uterus, while increasing the number of germ cell apoptosis in C. elegans. The apoptotic effects of TNT were blocked in mutants of cep-1 (w40), egl-1 (n487), and hus-1 (op241), indicating conserved genotoxic response genes was involved in mediating TNT-induced germ cell apoptosis. Parental exposure to TNT significantly increased the germ cell apoptosis from P0 to F2 generation, but the toxicity faded away in F3 and F4 generations. Furthermore, TNT was rapidly metabolized in P0, and the accumulation of 4-aminodinitrotoluene (4-ADNT), the main metabolite of TNT in C. elegans, showed a significant decrease from P0 to F1 and a slow decrease in the subsequent generations. Our results demonstrated that ingested TNT can cause severe transgenerational reproductive toxicity and be rapidly converted to 4-ADNT in the nematodes. These data provided basis for future studies on the effects of energetic compounds across generations.

Enhanced Uptake of Arsenic Induces Increased Toxicity with Cadmium at Non-Toxic Concentrations on Caenorhabditis elegans.

Cadmium (Cd) and arsenic (As) are widely distributed pollutants that co-exist in the environment; however, their joint toxicity on living organisms is still largely unknown. In this study, we explored the joint toxicity of concurrent exposure to Cd and different As species at low concentrations on Caenorhabditis elegans (C. elegans) in comparison to single exposures. Endpoints such as germ cell apoptosis, the number of oocytes, brood size, and the life span were employed to evaluate the combined effects of Cd and As on exposed C. elegans from L3 or L4 stages. Our results showed that concurrent exposure to non-toxic concentrations of Cd and As caused the synergy of reproductive and developmental toxicity. The presence of Cd promoted the accumulation of As in both germline and intestine detected by laser ablation inductively coupled plasma mass spectrometry (LA-ICP-MS). Although a conversion of As(III) to As(V) was detected as dependent on pH according to the microenvironment of the intestine in the worm, there was no significant difference of toxicity in C. elegans concurrently exposed to Cd and different As species. Using loss-of-function mutant strains, As was deemed responsible for the enhanced joint toxicity, and in which gcs-1 played a key protective role. These data help to better evaluate the comprehensive adverse effects of concurrent exposure of heavy metals at low concentrations on living organisms in the environment.