Regeneration of Tissue
Proliferation:
Replacement of lost cells by
mitosis
Replacement of the
extracellular matrix
Side reactions to
tissue injury
Side reactions to tissue injury
o Inflammation o Altered protein synthesis o Generalized reactions
It may be defined as harm induced capability of the organism for increased tolerance to harm itself. May result from biological changes and involves sensing noxious chemical and/or the initial damage or dysfuntion and a response that typically occurs through altered gene expression.
Adaptation
tissue death
Tissue necrosis
pathologic condition characterized by excessive deposition o an extracellular matrix of abnormal composition and is a specific manifestation of disrepair of the chronically injured tissue.
Fibrosis –
involves inappropriate function of various repair mechanisms including failure of DNA repair, failure of apoptosis, and failure to terminate cell proliferation.
Carcinogenesis
Mutation of
proto-oncogenes
Mutation tumo
supressor genes
appropriate activation or responsiveness of the regulatory region of critical genes
Epigenetic mechanisms in carcinogenesis
Promotion of Mutation and Clonal Growth
Failure of Apoptosis
Proto-oncogene Expression
Failure to Terminate Proliferation
Chemicals do not alter DNA or induce mutations yet induce cancer after chronic administration.
Nongenotoxic Carcinogens
Disposition Of Toxicants Composite actions of its
absorption, distribution, biotransformation, and elimination.
Main barriers:
skin, lungs, alimentary canal
The fraction absorbed or the rate of absorption is (), a chemical may never attain a sufficiently high concentration at a potential site of action to cause toxicity.
low
The distribution of a toxicant may be such that it is () in a tissue other than the target organ, thus decreasing toxicity.
concentrated
of a chemical may result in the formation of less toxic or more toxic metabolites at a fast or slow rate with obvious consequences for the concentration and, thus, the toxicity at the target site.
Biotransformation