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Arsenite exposure accelerates aging process regulated by the transcription factor DAF-16/FOXO in Caenorhabditis elegans.
Chemosphere 2016; 150:632-638C

Abstract

Arsenic is a known human carcinogen and high levels of arsenic contamination in food, soils, water, and air are of toxicology concerns. Nowadays, arsenic is still a contaminant of emerging interest, yet the effects of arsenic on aging process have received little attention. In this study, we investigated the effects and the underlying mechanisms of chronic arsenite exposure on the aging process in Caenorhabditis elegans. The results showed that prolonged arsenite exposure caused significantly decreased lifespan compared to non-exposed ones. In addition, arsenite exposure (100 μM) caused significant changes of age-dependent biomarkers, including a decrease of defecation frequency, accumulations of intestinal lipofuscin and lipid peroxidation in an age-dependent manner in C. elegans. Further evidence revealed that intracellular reactive oxygen species (ROS) level was significantly increased in an age-dependent manner upon 100 μM arsenite exposure. Moreover, the mRNA levels of transcriptional makers of aging (hsp-16.1, hsp-16.49, and hsp-70) were increased in aged worms under arsenite exposure (100 μM). Finally, we showed that daf-16 mutant worms were more sensitive to arsenite exposure (100 μM) on lifespan and failed to induce the expression of its target gene sod-3 in aged daf-16 mutant under arsenite exposure (100 μM). Our study demonstrated that chronic arsenite exposure resulted in accelerated aging process in C. elegans. The overproduction of intracellular ROS and the transcription factor DAF-16/FOXO play roles in mediating the accelerated aging process by arsenite exposure in C. elegans. This study implicates a potential ecotoxicological and health risk of arsenic in the environment.

Authors+Show Affiliations

Department of Bioenvironmental Systems Engineering, National Taiwan University, No. 1 Roosevelt Road, Sec. 4, Taipei 106, Taiwan.Department of Bioenvironmental Systems Engineering, National Taiwan University, No. 1 Roosevelt Road, Sec. 4, Taipei 106, Taiwan.Department of Bioenvironmental Systems Engineering, National Taiwan University, No. 1 Roosevelt Road, Sec. 4, Taipei 106, Taiwan. Electronic address: vivianliao@ntu.edu.tw.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

26796881

Citation

Yu, Chan-Wei, et al. "Arsenite Exposure Accelerates Aging Process Regulated By the Transcription Factor DAF-16/FOXO in Caenorhabditis Elegans." Chemosphere, vol. 150, 2016, pp. 632-638.
Yu CW, How CM, Liao VH. Arsenite exposure accelerates aging process regulated by the transcription factor DAF-16/FOXO in Caenorhabditis elegans. Chemosphere. 2016;150:632-638.
Yu, C. W., How, C. M., & Liao, V. H. (2016). Arsenite exposure accelerates aging process regulated by the transcription factor DAF-16/FOXO in Caenorhabditis elegans. Chemosphere, 150, pp. 632-638. doi:10.1016/j.chemosphere.2016.01.004.
Yu CW, How CM, Liao VH. Arsenite Exposure Accelerates Aging Process Regulated By the Transcription Factor DAF-16/FOXO in Caenorhabditis Elegans. Chemosphere. 2016;150:632-638. PubMed PMID: 26796881.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Arsenite exposure accelerates aging process regulated by the transcription factor DAF-16/FOXO in Caenorhabditis elegans. AU - Yu,Chan-Wei, AU - How,Chun Ming, AU - Liao,Vivian Hsiu-Chuan, Y1 - 2016/01/18/ PY - 2015/11/21/received PY - 2016/01/01/revised PY - 2016/01/04/accepted PY - 2016/1/23/entrez PY - 2016/1/23/pubmed PY - 2016/12/15/medline KW - Aging KW - Arsenic KW - Caenorhabditis elegans KW - DAF-16 KW - ROS SP - 632 EP - 638 JF - Chemosphere JO - Chemosphere VL - 150 N2 - Arsenic is a known human carcinogen and high levels of arsenic contamination in food, soils, water, and air are of toxicology concerns. Nowadays, arsenic is still a contaminant of emerging interest, yet the effects of arsenic on aging process have received little attention. In this study, we investigated the effects and the underlying mechanisms of chronic arsenite exposure on the aging process in Caenorhabditis elegans. The results showed that prolonged arsenite exposure caused significantly decreased lifespan compared to non-exposed ones. In addition, arsenite exposure (100 μM) caused significant changes of age-dependent biomarkers, including a decrease of defecation frequency, accumulations of intestinal lipofuscin and lipid peroxidation in an age-dependent manner in C. elegans. Further evidence revealed that intracellular reactive oxygen species (ROS) level was significantly increased in an age-dependent manner upon 100 μM arsenite exposure. Moreover, the mRNA levels of transcriptional makers of aging (hsp-16.1, hsp-16.49, and hsp-70) were increased in aged worms under arsenite exposure (100 μM). Finally, we showed that daf-16 mutant worms were more sensitive to arsenite exposure (100 μM) on lifespan and failed to induce the expression of its target gene sod-3 in aged daf-16 mutant under arsenite exposure (100 μM). Our study demonstrated that chronic arsenite exposure resulted in accelerated aging process in C. elegans. The overproduction of intracellular ROS and the transcription factor DAF-16/FOXO play roles in mediating the accelerated aging process by arsenite exposure in C. elegans. This study implicates a potential ecotoxicological and health risk of arsenic in the environment. SN - 1879-1298 UR - https://www.unboundmedicine.com/medline/citation/26796881/Arsenite_exposure_accelerates_aging_process_regulated_by_the_transcription_factor_DAF_16/FOXO_in_Caenorhabditis_elegans_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0045-6535(16)30004-2 DB - PRIME DP - Unbound Medicine ER -