Transgenerational reproductive and developmental toxicity of tebuconazole in Caenorhabditis elegans

Abstract

The transgenerational reproductive and developmental toxicity of tebuconazole (TEB) in Caenorhabditis elegans was investigated over five generations (P0 − F4). Only parental C.elegans (P0) were exposed to TEB (0, 0.01, 0.1, 1, and 10 μg/L) for 24 h and the subsequent offspring (F1-F4) were grown under TEB-free conditions. TEB exposure caused dose-dependent reproductive defects and developmental impairments in C.elegans. In the P0 generation reproductive defects were observed such as:reduced brood size and embryo hatchability, prolonged generation time, retarded gonadal development, and slower germline proliferation, even at 0.01 μg/L, together with developmental toxicity with significant reduced body length and narrowed body width at 10 μg/L. Additionally, the brood size significantly reduced in F2, which began to recover from F3, but was still lower than the control in F4. The proportion of abnormalities increased significantly in F2 and reduced from F3, but was still higher than the control, suggesting that TEB could have cumulative potential and be passed to offspring through parental exposure. Furthermore, exposure to TEB (10 μg/L) in P0 significantly reduced the body length in F1, which began to recover from F2, and was the same level as the control in F4. There was a concentrationdependent increase in body width in F1-F4, with a significant increase only observed in F1 at 10 μg/L. Thus, parental exposure to TEB induced transgenerational defects in both reproduction and development, emphasizing the significance of considering bio-toxicity over multiple generations to conduct accurate assessment of environmental risks of toxicants. K E Y W O R D SCaenorhabditis elegans, parental exposure, reproductive and developmental toxicity, Tebuconazole, trans-generation

A review of transgenerational and multigenerational toxicology in the in vivo model animal Caenorhabditis elegans

“…This assumption was confirmed by the observed damage on gonad development which was reflected by the length of the gonad arm, no eggs or vulva, abnormal oocytes, abnormal uterus, and relative area of the gonad arm after exposure to pollutants (Kim et al, 2013; Moon et al, 2017; Sun, Liao, et al, 2021). This assumption was also confirmed by the observations of elevated germline cell apoptosis, inadequate vitellogenin production, and slow germline proliferation in both P0 generation and subsequent descendant after exposure to pollutants (Li et al, 2018; Lu et al, 2020; Sun, Liao, et al, 2021; Yu et al, 2021).…”

“…As shown in Table 1, exposure to metals, organics, particle matters, and nanomaterials usually causes the reproductive toxicity reflecting by decreased offspring, prolonged generation time, and reproductive system abnormalities (such as impaired vulva development and retarded gonadal development) at both the P0 generation and the subsequent generations (Hu et al, 2008; Lu et al, 2020; Wang, Xie, et al, 2007). Inadequate vitellogenin production, BOW (bag of worms) phenotype, no eggs, increased germline apoptosis, and germline DNA damage were also detected in both the exposed P0 generation and the non‐exposed subsequent generations (Kim et al, 2013; Li et al, 2018; Lu et al, 2020). Generally, the brood sizes were decreased in P0 and F1, but some pollutants even reduced the brood size in F3 to F5 generations (Yu & Liao, 2016).…”

Towards a reporting guideline for developmental and reproductive toxicology testing in C. elegans and other nematodes

“…The most complete publications, reported on 26 out of 30 criteria [ 30 ] that we formulated, the most incomplete reported only 15 of 30 criteria [ 31 , 32 ] ( Fig. 1C ).…”

Reproductive Toxicity of Furfural Acetone in Meloidogyne incognita and Caenorhabditis elegans

“…Larval gonadal development assays were conducted as previously described [34]. Approximately 40 L 4 larvae of JK2868 nematodes were exposed to FAc in various concentrations for 24 h and then washed three times in sterile water.…”

“…Nematode treatment with active compounds or under stress could trigger germ-cell apoptosis, resulting in a reduction in germ-cell and brood size [23,26,34,38]. To determine whether exposure of FAc could induce the apoptotic response of germ-cell in C. elegans, AO staining assay was performed after nematode exposure to FAc for 24 h. As shown in Figure 4, 200 mg/L FAc exposure caused a significant increase in the number of apoptotic germ cells (0.6 at 0 mg/L and 3.5 at 200 mg/L; p < 0.001).…”