10.14: Cellular Toxicology
- Page ID
- 485531
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\(\newcommand{\avec}{\mathbf a}\) \(\newcommand{\bvec}{\mathbf b}\) \(\newcommand{\cvec}{\mathbf c}\) \(\newcommand{\dvec}{\mathbf d}\) \(\newcommand{\dtil}{\widetilde{\mathbf d}}\) \(\newcommand{\evec}{\mathbf e}\) \(\newcommand{\fvec}{\mathbf f}\) \(\newcommand{\nvec}{\mathbf n}\) \(\newcommand{\pvec}{\mathbf p}\) \(\newcommand{\qvec}{\mathbf q}\) \(\newcommand{\svec}{\mathbf s}\) \(\newcommand{\tvec}{\mathbf t}\) \(\newcommand{\uvec}{\mathbf u}\) \(\newcommand{\vvec}{\mathbf v}\) \(\newcommand{\wvec}{\mathbf w}\) \(\newcommand{\xvec}{\mathbf x}\) \(\newcommand{\yvec}{\mathbf y}\) \(\newcommand{\zvec}{\mathbf z}\) \(\newcommand{\rvec}{\mathbf r}\) \(\newcommand{\mvec}{\mathbf m}\) \(\newcommand{\zerovec}{\mathbf 0}\) \(\newcommand{\onevec}{\mathbf 1}\) \(\newcommand{\real}{\mathbb R}\) \(\newcommand{\twovec}[2]{\left[\begin{array}{r}#1 \\ #2 \end{array}\right]}\) \(\newcommand{\ctwovec}[2]{\left[\begin{array}{c}#1 \\ #2 \end{array}\right]}\) \(\newcommand{\threevec}[3]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \end{array}\right]}\) \(\newcommand{\cthreevec}[3]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \end{array}\right]}\) \(\newcommand{\fourvec}[4]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \\ #4 \end{array}\right]}\) \(\newcommand{\cfourvec}[4]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \\ #4 \end{array}\right]}\) \(\newcommand{\fivevec}[5]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \\ #4 \\ #5 \\ \end{array}\right]}\) \(\newcommand{\cfivevec}[5]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \\ #4 \\ #5 \\ \end{array}\right]}\) \(\newcommand{\mattwo}[4]{\left[\begin{array}{rr}#1 \amp #2 \\ #3 \amp #4 \\ \end{array}\right]}\) \(\newcommand{\laspan}[1]{\text{Span}\{#1\}}\) \(\newcommand{\bcal}{\cal B}\) \(\newcommand{\ccal}{\cal C}\) \(\newcommand{\scal}{\cal S}\) \(\newcommand{\wcal}{\cal W}\) \(\newcommand{\ecal}{\cal E}\) \(\newcommand{\coords}[2]{\left\{#1\right\}_{#2}}\) \(\newcommand{\gray}[1]{\color{gray}{#1}}\) \(\newcommand{\lgray}[1]{\color{lightgray}{#1}}\) \(\newcommand{\rank}{\operatorname{rank}}\) \(\newcommand{\row}{\text{Row}}\) \(\newcommand{\col}{\text{Col}}\) \(\renewcommand{\row}{\text{Row}}\) \(\newcommand{\nul}{\text{Nul}}\) \(\newcommand{\var}{\text{Var}}\) \(\newcommand{\corr}{\text{corr}}\) \(\newcommand{\len}[1]{\left|#1\right|}\) \(\newcommand{\bbar}{\overline{\bvec}}\) \(\newcommand{\bhat}{\widehat{\bvec}}\) \(\newcommand{\bperp}{\bvec^\perp}\) \(\newcommand{\xhat}{\widehat{\xvec}}\) \(\newcommand{\vhat}{\widehat{\vvec}}\) \(\newcommand{\uhat}{\widehat{\uvec}}\) \(\newcommand{\what}{\widehat{\wvec}}\) \(\newcommand{\Sighat}{\widehat{\Sigma}}\) \(\newcommand{\lt}{<}\) \(\newcommand{\gt}{>}\) \(\newcommand{\amp}{&}\) \(\definecolor{fillinmathshade}{gray}{0.9}\)Learning Objectives
After completing this lesson, you will be able to:
- Explain cellular adaptation.
- Identify four possible endpoints to toxic damage to cells and tissues.
- Define commonly used cancer terms.
- Describe the phases of and genetic activity associated with carcinogenesis.
- Identify mechanisms and potential outcomes of neurotoxicity.
In this section...
Topics include:
Section 14: Key Points
What We've Covered
This section made the following main points:
- To maintain homeostasis, cells and tissues undergo:
- Physiological adaptation, which is beneficial in nature — for example, increased skeletal muscle cells in athletes.
- Pathological adaptation, which is detrimental — for example, cellular changes in people who smoke cigarettes.
- Specific types of adaptation include:
- Atrophy — a decrease in the size of cells.
- Hypertrophy — an increase in the size of individual cells.
- Hyperplasia — an increase in the number of cells in a tissue.
- Metaplasia — the conversion from one type of mature cell to another type.
- Dysplasia — abnormal cell changes or deranged cell growth.
- Anaplasia — cells that are undifferentiated.
- Neoplasia — new growth of tissue.
- Most toxic effects, especially due to xenobiotics, are due to specific biochemical interactions without causing recognizable damage to a cell or its organelles. Cellular or biochemical toxicity leads to:
- The tissue being completely repaired and returned to normal.
- The tissue being incompletely repaired but capable of functioning with reduced capacity.
- Death of the organism or complete loss of a tissue or organ.
- Neoplasm or cancers.
- Tumors are either:
- Benign — similar to the cell of origin, slow-growing, and usually without systemic effects.
- Malignant — dissimilar from the cell of origin, rapid-growing, and commonly with systemic effects and life-threatening. Most malignant tumors are either:
- Carcinomas — arising in epithelium, the most common form of cancer, usually spread in the lymphatic system.
- Sarcomas — arising in connective or muscle tissue, usually spread by the blood stream.
- Carcinogenesis is a multi-step, multi-factorial genetic disease consisting of at least three main phases:
- Initiation — irreversible alteration of the DNA (mutation) of a normal cell.
- Promotion/Conversion — promoters enhance further development of the initiated cells, often influencing further expression of the mutated DNA such that the initiated cell proliferates and progresses further.
- Progression — development of the initiated cell into a biologically malignant cell population, often with metastasis to other areas of the body.
- Regulatory genes control the activity of structural genes and direct the proliferation process of the cell. Regulatory genes that play roles in carcinogenesis include:
- Proto-oncogenes — normal cellular genes that encode and instruct the production of regulatory proteins and growth factors within a cell or its membrane.
- Oncogenes — altered or misdirected proto-oncogenes with the ability to direct the production of proteins within the cell that change or transform the normal cell into a neoplastic cell.
- Tumor suppressor genes (anti-oncogenes) — present in normal cells and counteract and change the proto-oncogenes and altered proteins, preventing a cell with damaged DNA from proliferating and evolving into an uncontrolled growth.
- The p53 gene normally halts cell division, stimulates repair enzymes, and if necessary, commands the mutated cell to self-destruct
- p53 is the most frequently altered in human tumors and is incapable of its defense mechanisms
- Toxic damage to the nervous system is divided into three categories:
- Damage to sensory receptors and sensory neurons impacting the sensory functions.
- Damage to motor neurons causing muscular weakness and paralysis.
- Interneuronal damage causing learning deficiencies, memory loss, incoordination, and emotional conditions.