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Related Concept Videos

Teratogenicity01:07

Teratogenicity

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The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
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Cell division is necessary for growth and reproduction in organisms. Mitosis aids cell growth and development by dividing somatic cells. In contrast, meiosis causes the division of germ cells and plays an essential role in sexual reproduction. Due to their unique functional requirements, mitosis and meiosis differ from each other in multiple aspects.
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After a large-single-celled zygote is produced via fertilization, the process of cleavage occurs while zygotes travel through the uterine tube. Cleavage is a mitotic cell division that does not result in growth. With each round of successive cell division, daughter cells get increasingly smaller.
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Nondisjunction is the failure of homologous chromosomes or sister chromatids to separate correctly and move to the opposite poles of the cells. This produces daughter cells with abnormal chromosome numbers.  Nondisjunction is common during anaphase I or anaphase II of meiosis.  Mutations in synaptonemal complex proteins that attach homologous chromosomes increase the chances of nondisjunction in anaphase I of meiosis I. In contrast, mutations in topoisomerases and condensins that hold...
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Zygotic Development And Stem Cell Formation01:10

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The development of all multicellular organisms starts with the fusion of haploid cells called sperm and egg to form a diploid zygote. A zygote is a totipotent cell that can develop into a complete organism. The zygote undergoes cell division or cleavage to form an 8-cell mass. Until this stage, the cells are spherical, loosely attached, and remain totipotent. Totipotent cells are capable of developing both the embryonic and the extraembryonic tissues. However, as they continue to divide, they...
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In human women, oogenesis produces one mature egg cell or ovum for every precursor cell that enters meiosis. This process differs in two unique ways from the equivalent procedure of spermatogenesis in males. First, meiotic divisions during oogenesis are asymmetric, meaning that a large oocyte (containing most of the cytoplasm) and minor polar body are produced as a result of meiosis I, and again following meiosis II. Since only oocytes will go on to form embryos if fertilized, this unequal...
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Atomic Absorbance Spectroscopy to Measure Intracellular Zinc Pools in Mammalian Cells
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Atomic Absorbance Spectroscopy to Measure Intracellular Zinc Pools in Mammalian Cells

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Zinc deficiency and the developing embryo.

I E Dreosti1, I R Record, S J Manuel

  • 1Division of Human Nutrition, CSIRO (Australia), Kintore Avenue, 5000, Adelaide, South Australia.

Biological Trace Element Research
|November 22, 2013
PubMed
Summary
This summary is machine-generated.

Maternal zinc deficiency during pregnancy severely impacts fetal development, particularly the central nervous system, by disrupting DNA synthesis pathways. This study highlights critical developmental windows and interactions with other teratogens like alcohol.

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Area of Science:

  • Developmental biology
  • Nutritional science
  • Neuroscience

Background:

  • Zinc is crucial for fetal development, and its deficiency can lead to teratogenesis.
  • The central nervous system is particularly vulnerable to zinc deficiency during gestation.
  • Understanding the biochemical mechanisms and critical periods of zinc-related developmental effects is essential.

Purpose of the Study:

  • To review the effects of in utero zinc deficiency on fetal development in rats.
  • To investigate the biochemical lesions, especially in the central nervous system.
  • To explore interactions between zinc deficiency and other teratogens.

Main Methods:

  • Review of existing literature on zinc deficiency and fetal development in rats.
  • Analysis of biochemical pathways affected by zinc deficiency, including thymidine kinase.
  • Examination of the impact of dietary zinc restriction timing on teratogenesis.
  • Consideration of in vitro embryo culture and interactions with cadmium and alcohol.

Main Results:

  • Zinc deficiency depresses the thymidine kinase salvage pathway in fetal brain tissue, crucial for DNA synthesis.
  • A single 4-day period of zinc deficiency during critical morphogenesis (days 6-10) significantly impacts fetal abnormalities.
  • Maternal zinc status at term may be higher in dams with stunted pups due to early-pregnancy transient deficiency.
  • Zinc protects against cadmium-induced teratogenesis; alcohol and zinc deficiency interact, increasing fetotoxicity and lipid peroxidation.

Conclusions:

  • In utero zinc deficiency profoundly affects fetal development, with specific impacts on the central nervous system's DNA synthesis.
  • The timing of zinc deficiency during gestation is critical for the type and severity of teratogenic effects.
  • Interactions with environmental factors like alcohol exacerbate developmental toxicity, potentially through lipid peroxidation pathways.