PMID- 36933581
OWN - NLM
STAT- MEDLINE
DCOM- 20230411
LR  - 20230411
IS  - 1879-3177 (Electronic)
IS  - 0887-2333 (Linking)
VI  - 89
DP  - 2023 Jun
TI  - Oxidative stress-mediated mitochondrial apoptosis induced by the acaricide, 
      fenpyroximate, on cultured human colon cancer HCT 116 cells.
PG  - 105587
LID - S0887-2333(23)00036-X [pii]
LID - 10.1016/j.tiv.2023.105587 [doi]
AB  - Fenpyroximate (FEN) is an acaricide that inhibits mitochondrial electron 
      transport at the NADH-coenzyme Q oxidoreductase (complex I). The present study 
      was designed to investigate the molecular mechanisms underling FEN toxicity on 
      cultured human colon carcinoma cells (HCT116). Our data showed that FEN induced 
      HCT116 cell mortality in a concentration dependent manner. FEN arrested cell 
      cycle in G0/G1 phase and increased DNA damage as assessed by comet assay. 
      Induction of apoptosis was confirmed in HCT116 cells exposed to FEN by AO-EB 
      staining and Annexin V-FITC/PI double staining assay. Moreover, FEN induced a 
      loss in mitochondrial membrane potential (MMP), increased p53 and Bax mRNA 
      expression and decreased bcl2 mRNA level. An increase in caspase 9 and caspase 3 
      activities was also detected. All toghether, these data suggest that FEN induce 
      apoptosis in HCT116 cells via mitochondrial pathway. To check the implication of 
      oxidative stress in FEN-induced cell toxicity, we examined the oxidative stress 
      statue in HCT116 cells exposed to FEN and we tested the effect of a powerful 
      antioxidant, N-acetylcystein (NAC), on FEN-caused toxicity. It was observed that 
      FEN enhanced ROS generation and MDA levels and disturbed SOD and CAT activities. 
      Besides, cell treatment with NAC significantly protected cells from mortality, 
      DNA damage, loss of MMP, and caspase 3 activity induced by FEN. To the best of 
      our knowledge, this is the first study showing that FEN induced mitochondrial 
      apoptosis via ROS generation and oxidative stress.
CI  - Copyright (c) 2023 Elsevier Ltd. All rights reserved.
FAU - Ayed-Boussema, Imen
AU  - Ayed-Boussema I
AD  - Laboratory of Research on Biologically Compatible Compounds, LR01SE17 University 
      of Monastir, Faculty of Dental Medicine, 5019 Monastir, Tunisia; Faculty of 
      Sciences of Gafsa, University of Gafsa, Tunisia. Electronic address: 
      imen.ayed333@gmail.com.
FAU - Rjiba-Touati, Karima
AU  - Rjiba-Touati K
AD  - Laboratory of Research on Biologically Compatible Compounds, LR01SE17 University 
      of Monastir, Faculty of Dental Medicine, 5019 Monastir, Tunisia; Faculty of 
      Sciences of Gafsa, University of Gafsa, Tunisia.
FAU - Hamdi, Hiba
AU  - Hamdi H
AD  - Laboratory of Research on Biologically Compatible Compounds, LR01SE17 University 
      of Monastir, Faculty of Dental Medicine, 5019 Monastir, Tunisia.
FAU - Chaabani, Hanen
AU  - Chaabani H
AD  - Laboratory of Research on Biologically Compatible Compounds, LR01SE17 University 
      of Monastir, Faculty of Dental Medicine, 5019 Monastir, Tunisia.
FAU - Abid-Essefi, Salwa
AU  - Abid-Essefi S
AD  - Laboratory of Research on Biologically Compatible Compounds, LR01SE17 University 
      of Monastir, Faculty of Dental Medicine, 5019 Monastir, Tunisia.
LA  - eng
PT  - Journal Article
DEP - 20230317
PL  - England
TA  - Toxicol In Vitro
JT  - Toxicology in vitro : an international journal published in association with 
      BIBRA
JID - 8712158
RN  - 0 (Acaricides)
RN  - 9W557V4RYA (fenpyroximate)
RN  - 0 (Reactive Oxygen Species)
RN  - EC 3.4.22.- (Caspase 3)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Humans
MH  - HCT116 Cells
MH  - *Acaricides/pharmacology
MH  - Reactive Oxygen Species/metabolism
MH  - Caspase 3/metabolism
MH  - Oxidative Stress
MH  - *Colonic Neoplasms
MH  - Apoptosis
MH  - RNA, Messenger/metabolism
MH  - Membrane Potential, Mitochondrial
OTO - NOTNLM
OT  - Apoptosis
OT  - Cell cycle arrest
OT  - DNA damage
OT  - Fenpyroximate
OT  - Mitochondrial pathway
OT  - Oxidative stress
COIS- Declaration of Competing Interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2023/03/19 06:00
MHDA- 2023/04/11 06:41
CRDT- 2023/03/18 20:27
PHST- 2023/01/16 00:00 [received]
PHST- 2023/03/02 00:00 [revised]
PHST- 2023/03/15 00:00 [accepted]
PHST- 2023/04/11 06:41 [medline]
PHST- 2023/03/19 06:00 [pubmed]
PHST- 2023/03/18 20:27 [entrez]
AID - S0887-2333(23)00036-X [pii]
AID - 10.1016/j.tiv.2023.105587 [doi]
PST - ppublish
SO  - Toxicol In Vitro. 2023 Jun;89:105587. doi: 10.1016/j.tiv.2023.105587. Epub 2023 
      Mar 17.