Cytotoxicity of nitrogenous disinfection byproducts: A combined experimental and computational study

Hong, Huachang; Lu, You; Zhu, Xiaoyan; Wu, Qiang; Jin, Lingmin; Zhang, Jin; Wei, Xiaoxuan; Ma, Guangcai; H, Yu

doi:10.1016/j.scitotenv.2022.159273

Cited by 24 publications

(6 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…13,15 These results indicated that the position and number of bromine atoms can impact the toxic potencies of brominated CZ. Similar cases were also reported by Hong et al, 29 which pointed out that the addition of halogen exacerbates the toxicity of aromatic components. This is probably due to the addition of halogen can increase the bioconcentrations of aromatic components and then generate more reactive oxygen species in the organism.…”

Section: Lethal Effect Of 3-bcz On Zebrafish At the Early Life Stagesupporting

confidence: 86%

3-Bromocarbazole-Induced Developmental Neurotoxicity and Effect Mechanisms in Zebrafish

et al. 2023

Self Cite

View full text Add to dashboard Cite

Polyhalogenated carbazoles (PHCZs) are dioxinlike emerging contaminants, but limited information exists on their neurotoxicity and mechanisms. This study employed zebrafish embryos to investigate the adverse effects of 3-bromocarbazole (3-BCZ), a typical PHCZ, exposure in their early life stages and found that the 120 h post fertilization (hpf)-median lethal concentration (LC 50 ) value of 3-BCZ in zebrafish larvae was 2.88 mg/L. The results revealed that 3-BCZ inhibited tail coiling at ≥0.06 mg/L, decreased hatchability at ≥2.88 mg/L, increased mortality and malformation rates at ≥1.44 mg/L, induced aryl hydrocarbon receptor effects and reduced body length at ≥0.58 mg/L, and inhibited behavior activities at ≥0.06 mg/L. Further mechanism investigations showed that 3-BCZ exposures repressed the motor neuron axon length via downregulating the mRNA transcription levels of α1-tubulin, Gap43, Syn2a, and shha, and decreased central nervous system neurogenesis via downregulating the mRNA transcription levels of elavl3, nrd, mbp, and gfap. Overall, 3-BCZ induces developmental neurotoxicity in zebrafish larvae at 0.06 mg/L (1/50 LC 50 ). Tail coiling activity at 24 hpf and swimming total distance at 120 hpf could be ideal indicators of 3-BCZ health risks in zebrafish. These findings provide valuable insights for health and ecological risk assessments of 3-BCZ and other PHCZs.

show abstract

Section: Lethal Effect Of 3-bcz On Zebrafish At the Early Life Stagesupporting

confidence: 86%

3-Bromocarbazole-Induced Developmental Neurotoxicity and Effect Mechanisms in Zebrafish

et al. 2023

Self Cite

View full text Add to dashboard Cite

show abstract

“…Among them, trihalomethanes and haloacetic acids are the most abundant, and have been regulated by many countries and regions (Richardson et al, 2007;Ding et al, 2013;Lin et al, 2018;Zheng et al, 2020;Weng et al, 2022). Nitrogenous and iodinated DBPs such as haloacetamide (HAcAms) are usually in low levels in drinking water and have not been regulated (Krasner et al, 2006;Ding et al, 2013;Dong et al, 2019), yet it has attracted much attention due to its extremely high cytotoxicity and genotoxicity (Richardson et al, 2007;Wagner and Plewa 2017;Hong et al, 2023). Many studies have been carried out on the toxicity of haloacetonitriles since the 1980s (Lin et al, 1986;Ahmed et al, 1989;Ahmed et al, 1991;Lipscomb et al, 2009;Komaki et al, 2014;Dong et al, 2018b), but the toxicology research on HAcAms, especially on iodinated haloacetamides (I-HAcAms), remained sparse.…”

Section: Introductionmentioning

confidence: 99%

Untitled

2023

WATER

View full text Add to dashboard Cite

Iodoacetamide (IAcAm) is a type of emerging nitrogenous disinfection by-product (N-DBP) with high health risk. Up to now, several studies have been carried out on the toxicity of IAcAm, but the study on oxidative damage of IAcAm on human cells was not available. In this study, the oxidative stress and damage induced by IA-cAm on HepG-2 cells were investigated. Results showed that superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity exhibited a decreasing trend; but nuclear factor erythroid 2-related factor 2 (NRF2) and glutamate cysteine ligase catalytic subunit (GCLC), both the mRNA and protein level, generally appeared an increasing trend with the increase of IAcAm concentration. These results suggested that IAcAm-exposed cells produced excessive reactive oxygen species (ROS) and initiated the compensation mechanism of NRF2 to deal with oxidative stress. Malonaldehyde (MDA), an index for oxidative damage, had no obvious change at 24 h (p>0.05) but signifi cantly increased at 48 h (p<0.05). This result indicated that HepG-2 cells could protect themselves from ROS attack by consuming antioxidant enzyme (e.g., SOD and GSH-Px) and upregulating the genes related to antioxidation after 24 h exposure of IA-cAm; yet, at 48 h, the antioxidant defense system could no longer prevent oxidative damage of ROS, causing severe damage of the lipid membrane.

show abstract

“…1,2 To date, more than 700 DBPs were identified in drinking water, of them, trihalomethanes and haloacetic acids had been classified as the regulated DBPs in drinking water due to their frequent occurrence and higher health risks. [3][4][5] Although some emerging DBPs levels is far lower than that of regulated DBPs, they have been proved to be more toxic than regulated DBPs, thus the presence of emerging DBPs in water pose potential health risk on public health. 6,7 2,6-dichloro-1,4-benzoquinone (2,6-DCBQ) is one of emerging DBPs, which has been so far detected and identified in various waters (drinking water, swimming water, and treated water), the frequent occurrence of 2,6-DCBQ have attracted more attentions.…”

Section: Introductionmentioning

confidence: 99%

“…Disinfection byproducts (DBPs), are unintendedly produced from the reaction of disinfectants with dissolved organic matter (DOM) in water, which have been regarded as a considerable threat to public health 1,2 . To date, more than 700 DBPs were identified in drinking water, of them, trihalomethanes and haloacetic acids had been classified as the regulated DBPs in drinking water due to their frequent occurrence and higher health risks 3–5 . Although some emerging DBPs levels is far lower than that of regulated DBPs, they have been proved to be more toxic than regulated DBPs, thus the presence of emerging DBPs in water pose potential health risk on public health 6,7 …”

Section: Introductionmentioning

confidence: 99%

Molecular insights of 2,6‐dichlorobenzoquinone‐induced cytotoxicity in zebrafish embryo: Activation of ROS‐mediated cell cycle arrest and apoptosis

Dong

Ding

Liu

et al. 2022

Environmental Toxicology

Self Cite

View full text Add to dashboard Cite

2,6‐dichloro‐1,4‐benzoquinone (2,6‐DCBQ), as an emerging disinfection by‐product, has been frequently detected in waters, posing potential health risk on public health. Although some studies have pointed out that 2,6‐DCBQ exposure can induce cytotoxicity, limited information is available for underlying mechanism for 2,6‐DCBQ‐induced cytotoxicity. To explore this mechanism, we assessed the levels of reactive oxygen species (ROS), acridine orange (AO) staining, and the mRNA transcriptions of genes (Chk2, Cdk2, Ccna, Ccnb and Ccne) involved in cell‐cycle and genes (p53, bax, bcl‐2 and caspase 3) involved in apoptosis in zebrafish embryo, after exposed to different concentrations (10, 30, 60, 90 and 120 μg/L) of 2,6‐DCBQ for 72 h. Our results indicated that 2,6‐DCBQ exposure induced ROS generation and cell apoptosis, and disturbed the mRNA transcription of genes related to cell cycle and apoptosis in zebrafish embryo. Moreover, we also found that 30 ~ 60 μg/L 2,6‐DCBQ is the important transition from cell‐cycle arrest to cell apoptosis. These results provided novel insight into 2,6‐DCBQ‐induced cytotoxicity.

show abstract

Cytotoxicity of nitrogenous disinfection byproducts: A combined experimental and computational study

Cited by 24 publications

References 61 publications

3-Bromocarbazole-Induced Developmental Neurotoxicity and Effect Mechanisms in Zebrafish

3-Bromocarbazole-Induced Developmental Neurotoxicity and Effect Mechanisms in Zebrafish

Untitled

Molecular insights of 2,6‐dichlorobenzoquinone‐induced cytotoxicity in zebrafish embryo: Activation of ROS‐mediated cell cycle arrest and apoptosis

Contact Info

Product

Resources

About