Role of gene expression in mechanisms of toxicity/carcinogenicity relative to environmental cancer, heart, and lung disease

Abstract

DNA damage may be one of a large number of mechanisms initiating acute heart and lung disease, and may be a major mechanism initiating long‐latency heart and lung disease. Gene expression can modulate metabolism, DNA damage, DNA repair, DNA replication, and expression of mutation. Conversely, DNA damage appears capable of altering gene expression. Environmental long‐latency heart and lung disease, in analogy to cancer, may exhibit: heart and lung as targets for some environmental agents and non‐targets for others; hormone‐ and development‐dependent heart and lung disease; and two‐stage initiation‐promotion phenomena.

Key words:

• Long‐latency disease
• metabolism
• DNA damage
• DNA repair
• DNA replication
• tumor promotion