Toxic effects of thallium acetate by acute exposure to the nematode C. elegans

Thallium (Tl) is a toxic metalloid and an emerging pollutant due to electronic devices and dispersal nearby base-metal mining. Therefore, Tl poses a threat to human health and especially the long-term impact on younger individuals exposed is still unknown. This study aimed to evaluate the toxic effects of thallium acetate in C. elegans in early larval stages, considering physiological and behavioral endpoints, as well as the Tl absorption and bioaccumulation.

Caenorhabditis elegans (C. elegans) was exposed to Thallium acetate (50, 100, 150, 200, 250, 500, and 1000 μM) in the L1 larval stage, with the purpose to observe the toxic effects invoked until adulthood. Transgenic worms strains were transported GFP, reporters to DAF-16 and were used to verify the antioxidant response. ICP-MS quantified total Tl⁺ concentration to evidence Tl uptake and bioaccumulation.

Thallium acetate caused a significant reduction in the number of living worms (p < 0.0001 in 100-1000 μM), a delay in larval development (p < 0.01; p < 0.001 and p < 0.0001 in 100-1000 μM) through the larval stages, and egg production in the worm's uterus was reduced. Thallium acetate also induced behavioral changes. Additionally, thallium acetate activated antioxidant pathway responses in C. elegans by translocating the DAF-16 transcription factor and activation of SOD-3::GFP expression. The Tl⁺ quantification in worms showed its absorption in the L1 larval stage and bioaccumulation in the body after development.

Thallium acetate reduced survival, delayed development, caused behavioral changes, induced responses inherent to oxidative stress, and serious damage to the worm's reproduction. In addition, C. elegans absorbed and bioaccumulated Tl⁺. Together, our results highlight the impacts of Tl⁺ exposure in the early stages of life, even for a short period.