AI Article Synopsis
- Exposure to arsenic (As) poses serious health risks and alters cellular processes, triggering apoptosis in affected individuals.
- A study sequenced the mitochondrial genome of individuals exposed to As and found specific mutations that could lead to mitochondrial dysfunction, rather than large-scale DNA changes.
- Results indicated that the harmful mutations in mitochondrial Complex I correlated with increased reactive oxygen species (ROS) levels and significant cell cycle arrest, highlighting the toxic impact of arsenic exposure.
Article Abstract
Exposure to arsenic (As) causes serious health hazards. Therefore, there is a sustained effort to understand the molecular basis of the risk posed by the toxicant. It has been reported that apoptotic changes ensue on exposure to As. To investigate the molecular basis of such changes, we sequenced the entire mitochondrial (mt) genome from PBMC of a subset of these individuals (As-exposed=16 and unexposed=18) using Affymetrix platform. Our analysis revealed that As exposure does not induce large-scale mt-DNA variations, but that specific deleterious changes could induce mt dysfunction. A Glu115Ter mutation as well as 17 other in silico predicted deleterious variants were identified exclusively in exposed individuals. The number of variants in mt Complex I in As-exposed individuals was positively correlated with their respective intracellular ROS level. In addition, the extent of potentially damaging variants in As-exposed individuals had significant positive correlation to the degree of G0 /G1 cell cycle arrest.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/em.21828 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!