The Molecular Mechanisms of Adaptive Response Related to Environmental Stress.
Andrea RossnerovaAlberto IzzottiAlessandra PullieroAalt BastS I S RattanPavel RossnerPublished in: International journal of molecular sciences (2020)
The exposure of living organisms to environmental stress triggers defensive responses resulting in the activation of protective processes. Whenever the exposure occurs at low doses, defensive effects overwhelm the adverse effects of the exposure; this adaptive situation is referred to as "hormesis". Environmental, physical, and nutritional hormetins lead to the stimulation and strengthening of the maintenance and repair systems in cells and tissues. Exercise, heat, and irradiation are examples of physical hormetins, which activate heat shock-, DNA repair-, and anti-oxidative-stress responses. The health promoting effect of many bio-actives in fruits and vegetables can be seen as the effect of mildly toxic compounds triggering this adaptive stimulus. Numerous studies indicate that living organisms possess the ability to adapt to adverse environmental conditions, as exemplified by the fact that DNA damage and gene expression profiling in populations living in the environment with high levels of air pollution do not correspond to the concentrations of pollutants. The molecular mechanisms of the hormetic response include modulation of (a) transcription factor Nrf2 activating the synthesis of glutathione and the subsequent protection of the cell; (b) DNA methylation; and (c) microRNA. These findings provide evidence that hormesis is a toxicological event, occurring at low exposure doses to environmental stressors, having the benefit for the maintenance of a healthy status.
Keyphrases
- dna damage
- dna repair
- human health
- heat shock
- dna methylation
- air pollution
- physical activity
- mental health
- genome wide
- life cycle
- transcription factor
- heat stress
- oxidative stress
- risk assessment
- induced apoptosis
- gene expression
- healthcare
- cell therapy
- heavy metals
- cell cycle arrest
- gram negative
- copy number
- dna damage response
- heat shock protein
- cystic fibrosis
- multidrug resistant
- social media
- health risk
- cell death
- electronic health record
- particulate matter
- health risk assessment