Dimethachlor is a chloroacetanilide herbicide that interferes with the synthesis of very long-chain fatty acids (VLCFAs) in target plants (Yang et al., 2010). Because VL-CFAs are important lipid components in seeds and surface covering materials, such as plant waxes (von Wettstein-Knowles, 1993;Cassagne et al., 1994), compounds of the chloroacetanilide family have been used in crop production for more than 50 years (Junghans et al., 2003). Although these herbicides effectively increase agricultural productivity via the regulation of unwanted weeds, they have caused environmental pollution by leaching. For example, other chloroacetanilides, such as acetochlor, alachlor, and metolachlor, are detectable in surface water samples from rivers and streams (Battaglin et al., 2000). In the case of dimethachlor, its water solubility is 2,300 mg/ L; thus, a large amount of dimethachlor dissolves in water (Lewis et al., 2016). As the exposure of aquatic ecosystems to dimethachlor is highly probable because dissolved herbicides can leach with water flow (Ferreira Mendes et al., 2020), it is necessary to identify whether dimethachlor has a harmful effect on aquatic organisms.

High levels of proinflammatory cytokines have been observed in obese pregnancies. Obesity during pregnancy may increase the risk of various pregnancyrelated complications, with pathogenesis resulting from excessive inflammation. Palmitic acid (PA) is a saturated fatty acid that circulates in high levels in obese women. In our previous study, we found that PA inhibited the proliferation of trophoblasts developing into the placenta, induced apoptosis, and regulated the number of cleaved halves derived from transfer RNAs (tRNAs). However, it is not known how the expression of tRNA-derived stress-induced RNAs (tiRNAs) changes in response to PA treatment at concentrations that induce inflammation in human trophoblasts. We selected concentrations that did not affect cell viability after dose-dependent treatment of HTR8/SVneo cells, a human trophoblast cell line. PA (200 μM) did not affect the expression of apoptotic proteins in HTR8/SVneo cells. PA significantly increased the expression of inflammatory cytokines including interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α. In addition, 200 μM PA significantly increased the expression of tiRNAs compared to 800 μM PA treatment. These results suggest that PA impairs placental development during early pregnancy by inducing an inflammatory response in human trophoblasts. In addition, this study provides a basis for further research on the association between PA-induced inflammation and tiRNA generation.

To regulate the growth of broad leaf weeds in crop fields, chlorophenoxy herbicides, including dicamba, mecoprop, mecorpop-p, and 4-chloro-2-methylphenoxyacetic acid, are widely used (Sanchis et al., 2013;Mottier et al., 2014). The toxicities of several chlorophenoxy herbicides have been reported despite their widespread use. For example, 2,4-dichlorophenoxyacetic acid can cause cerebrovascular impairments in rats by damaging the structure of the plasma membrane (Elo et al., 1988;Bradberry et al., 2000). Mecoprop-p, another chlorophenoxy herbicide, is a synthetic auxin that has been widely used to control weed growth since the 1980s (Périllon et al., 2021). It is known to be poorly absorbed in the soil but has a high water solubility of 250 mg/L at 20℃

Norflurazon is widely used on agricultural lands and has a high potential to pollute water sources. However, its effects on fish have not been fully elucidated. The purpose of our study was to determine whether norflurazon adversely affects the developmental stage of zebrafish, which are frequently used as a model system to evaluate the environmental impact of pollutants. Norflurazon interfered with the hatching of zebrafish embryos and induced several sublethal deformities including body length reduction, increased yolk sac volume, and enlargement of the pericardial region. We further examined the cardiotoxicity of norflurazon in the flk1:eGFP transgenic zebrafish line. The vascular network, mainly in the brain region, was significantly disrupted in norflurazon-exposed zebrafish. In addition, due to the failure of cardiac looping, norflurazon-exposed zebrafish had an abnormal cardiac structure. These developmental abnormalities were related to the apoptotic process triggered by norflurazon. Overall, the present study demonstrated the non-target toxicity of norflurazon by analyzing the hazardous effects of norflurazon on developing zebrafish.