thallium is a rare metal used in the electronics industry. its toxic effects have already been observed in humans and the nematode caenorhabditis elegans (c. elegans). this study evaluated the effects of thallium acetate on the behavior of c. elegans and antioxidant response. adult worms wee synchronized and remain in
m9 buffer for approximately 24 h, to obtain worms only in
l1 stage larval. the worms
l1 were exposed to thallium acetate in concentrations of 50, 100, 150, 200, 250, 500, and 1000 microm for 1 h. after that, worms were transferred to new ngm plates with bacteria and allowed until the
l4 larval stage. animals were tested for survival, 24 h next to the exposure, and the pharyngeal pumping and the defecation cycles, in
l4 stage. the larval development was monitored from
l1 larval stage until adulthood and body bend assays were performed in individual worms, during 20 s, into a plate without bacteria. after one min of adaptation, worms were scored for the number of body bends performed in 20 s. the reproductive capacity of the animals was also evaluated, by counting eggs from individual worms. the subcellular localization of
daf-16 and expression of sod in stress response were evaluated in a fluorescence microscope. the amount of tl+ was determined in
l1 stage worms using icp-ms. the worms were survival affected after 100 microm to 1000 microm exposure and absence or reduction of contractions in the pharyngeal muscles was observed in worms treated at 1000 microm. acute exposure to thallium acetate altered the peristaltic movement in the intestinal tract of worms of 500 to 1000 microm. the c. elegans exposed remained paralyzed for a few minutes after the treatment, which could positively impact the developmental delay. the results showed a significant increase in body movement. there was a significant reduction in egg-production at concentrations above 100 microm, suggesting that thallium acetate also affects the worm's reproductive system. in the
l1 larval stage worms, there was a significant activation of the antioxidant pathway, evidenced by the translocation of
daf-16 from the cytosol to the nuclear region, but in the
l4 larval stage, there was no translocation.
sod-3 expression was only evidenced in the exposed worms
l4 stage, indicates an activation of the antioxidant response to thallium acetate. the tl+ body load increased in a dose-dependent manner, after the development of the worm, part of the tl+ was not excreted, bioaccumulating in the body at lower levels. in this study, we verified new information concerning the toxicity induced by thallium acetate, using c. elegans. we recognize that additional studies are needed to clarify the mechanisms underlying the adverse effects of thallium, and the possible neural damage caused.