Telomeres susceptibility to environmental arsenic exposure: Shortening or lengthening?

Abstract

Maintaining telomere length plays a crucial role in regulating cellular life span. Telomere lengthening or shortening is one of the important biomarkers which could predict the preceding or present diseases. Meanwhile, the impact of environmental arsenic exposure on telomere length has increasingly concerned. Although previous studies demonstrated the effects of arsenic on telomere length, the findings were unclear on whether telomere shortens or lengthens by arsenic exposure. Thus, this manuscript summarized and discussed the telomere length alteration following arsenic exposure and the possible does-response effect of arsenic on telomere length. The present review suggested that different age groups may respond differently to arsenic exposure, and the dose-response effect of arsenic could be a critical factor in its effect on telomere length. Moreover, speciation analysis of arsenic could be more informative in identifying the effect of arsenic on telomere length.

Telomere dynamics and oxidative stress in Arabidopsis grown in lunar regolith simulant

“…Interestingly, phytoremediation can also mitigate the negative consequences of heavy metals (Yan et al, 2020). There is extensive literature linking heavy metals to telomere length changes (Pawlas et al, 2015;Zota et al, 2015;Borghini et al, 2016;Fillman et al, 2016;Wai et al, 2020;Wai et al, 2023). Since heavy metal exposure elevates ROS (Flora, 2002;Cuypers et al, 2010;Jaishankar et al, 2014), one intriguing possibility is the heavy metal content of the lunar regolith simulant (Long-Fox et al, 2023) causes increased genome oxidation, which in turn leads to telomere shortening.…”

Cellular senescence in asthma: from pathogenesis to therapeutic challenges

“… 19 Telomeres at the ends of chromosomes comprise repeat sequences (TTAGGG) that shorten with each cell division because of the nature of the DNA replication machinery. 20 They protect against chromosomal damage by preventing chromosome–chromosome fusions and degradation and subsequently maintaining genome integrity. 21 Telomere shortening occurs in normal somatic cells following each cell division.…”

Mechanisms of genotoxicity and proteotoxicity induced by the metalloids arsenic and antimony

“…Epidemiological studies reported both lengthening and shortening of telomeres in individuals chronically exposed to As(III) [ 85 ]. A possible mechanism for As(III)-induced telomere lengthening involves the upregulation of the telomerase catalytic subunit (hTERT) and telomere binding proteins such as TRF1 and TRF2, subunits of the telomere sheltering complex [ 85 ]. Thus, As(III) may partially contribute to carcinogenesis by promoting telomere elongation, which is crucial for the maintenance and viability of human cancer cells.…”

“…Paradoxically, As(III)-induced downregulation of both hTERT and TRF2 was also observed and associated with telomere shortening. Since telomere sequences are rich in guanine, which is particularly sensitive to oxidative damage, it has been proposed that As(III) may cause telomere attrition through oxidative stress [ 85 ]. Importantly, 4 μM As(III) induced increased ROS levels in glioblastoma cells (U87 line) followed by translocation of telomerase from the nucleus to the cytoplasm, telomere shortening, and accumulation of γH2AX (histone H2AX variant phosphorylated on Ser139, which serves as a sensitive marker of DNA damage and repair) that co-localized with TRF1, strongly suggesting that the telomeres are sites of As(III)-generated DNA damage in an oxidative stress-dependent manner [ 86 ].…”