Teratogens essay

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Teratogens essay

Since the s the accumulation of spontaneous mutations in the DNA of organs and tissues has been hypothesized to underlie aging itself e. What are mutations, and why are they there? DNA damage consists of chemical alterations in DNA structure, leading to a structure that can no longer serve as a substrate for faithful replication or transcription.

DNA damage cannot be copied to end up in daughter cells.

Teratogens essay

DNA mutations are heritable changes in a DNA sequence of an organism, which can be part of a gene, a gene regulatory region, or some noncoding part of the genome. Mutations are usually introduced as a consequence of misreplication or misrepair, for example, due to the presence of DNA damage.

Hence, DNA damage can lead to mutations when it is not correctly repaired. Mutations can vary from point mutations, involving single or very few base pairs to large deletions, insertions, duplications, and inversions.

Mutation | regardbouddhiste.com

In organisms with multiple chromosomes, DNA from one chromosome can be joined to another and the actual chromosome number can be affected. Indeed, they fuel the survival of cells and organisms in times of stress.

They are the substrate for evolution, which gave rise to different life forms. In both prokaryotic and eukaryotic cells mutation rate can be greatly increased, causing many cells to die but also giving rise to cells with the necessary attributes to survive and expand.

Teratogens essay

Cancer cells, for example, can undergo mutations in genes that control the mutation rate for example, genes involved in DNA repair. Such "mutator phenotypes" allow them to accelerate the acquisition of novel attributes e.

While in such cases mutations are detrimental for the host, they are beneficial for the cell. In most cases, mutations will have adverse effects on both the host and the cell.

In the somatic cells of multicellular organisms, however, mutations usually have adverse effects. Gross chromosomal alterations The earliest and still the most popular way to look at mutations is by cytogenetic means.

This necessarily precludes the detection of mutational events smaller than a few million base pairs and also limits the target tissue to cells in metaphase, usually white blood cells.

A noteworthy exception to this latter limitation is the original work of the late Howard Curtiswho with coworkers examined mouse liver parenchymal cell metaphase plates after partial hepatectomy and found considerably higher numbers of cells with abnormal chromosomes in old, compared with young, animals i.

Later, large structural changes in DNA were observed to increase with donor age in white blood cells of human individuals, from about 2—4 percent of the cells having chromosomal aberrations in young individuals to about six times higher in the elderly.

The recent use of more advanced methods, such as chromosome painting, have confirmed the increase in cytogenetic damage with age in both human and mouse. In both human and mouse lymphocytes the increase in chromosome aberrations appeared to be exponential.

Mutations detected in selectable marker genes With the development of tests based on selectable endogenous marker genes, it became possible to assess mutation frequencies at these loci in T-cells from human and animal donors for a review see Vijg, Using the hypoxanthine phosphoribosyl transferase HPRT locus test, investigators have shown that mutation frequencies at this locus increase with donor age.

In mice mutation frequencies have been reported from about 5 x in young animals to about 3 x in middle aged mice Dempsey et al. However, in both mice and humans these values could be underestimates, due to the loss of HPRT mutants in vivo or in vitro.

Indeed, results from Grist et al.

Values higher than HPRT were also found with other assays involving selectable target genes. The discrepancy has been explained in terms of the inability of the HPRT test to detect mitotic recombination events HPRT is X-linked and a relatively strong in vivo selection against mutants.

In mice subjected to caloric restriction, the only intervention demonstrated to increase life span Masoro,HPRT mutation frequencies were found to increase with age at a significantly slower rate than in the animals that fed at will.Evolutionary Psychology.

In its broad sense, the term "evolutionary psychology" stands for any attempt to adopt an evolutionary perspective on human behavior by supplementing psychology with the central tenets of evolutionary biology.


The underlying idea is that since our mind is the way it is at least in part because of our evolutionary past, evolutionary theory can aid our understanding not.

Evolution Genetics Biostatistics Population Genetics Genetic Epidemiology Epidemiology HLA MHC Inf & Imm Homepage. Common Terms in Genetics. regardbouddhiste.com DORAK. Please.

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Teratogens Essays: Over , Teratogens Essays, Teratogens Term Papers, Teratogens Research Paper, Book Reports. ESSAYS, term and research papers available for . Abnormal Psychology Mood Disorders - Abnormal Psychology-Mood Disorders The study of abnormal behavior in which deviates from the social norms of an individual human being, With the potential to affect our Psychological development is known as Abnormal Psychology.

No Teratogens During Pregancy Essay Words | 5 Pages A teratogen is any agent or factor that can disrupt the development of an embryo or fetus, which may cause a birth defect or malformation.

No Teratogens During Pregancy Essay Words | 5 Pages A teratogen is any agent or factor that can disrupt the development of an embryo or fetus, which may cause a birth defect or malformation.

Common Terms in Genetics [regardbouddhiste.com DORAK]