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Paper Animal Development
Complexity in Animals Further Development:
Normal and Abnormal Development
Compiled by:
M. Syawal 40934201
Rilly Andika 40934202
Shofia lubis 40934203
Suciati Primasari 40934203
Wiwik Simanjuntak 40934203
MATHEMATIC AND NATURAL SCIENCE FACULTY
STATE UNIVERSITY OF MEDAN
2011
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INTRODUCTION
On the Animal Development lecture, we have studied the early embryo development. In
addition we also learn about the animal further development. So in order to fulfill the
assignment of animal development lecture, then we write a paper about normal and
abnormal animal development, also about teratogenesis and teratogens substances.
In normal animal development, one can usually distinguish 4 stages of embryonic
development. There is cleavage-patterning-differentiation-growth.
But during embryonic period, abnormality development possible to take places which is
caused by either genetic or environmental factors and then abnormal development lead
to changes in form and structure.
DISCUSSION
* Normal and abnormal development
If a number of fertilized eggs of a given species are provided with conditions that
enable them to develop at all, they will, with extraordinary regularity, develop into
exceedingly similar adult organisms. The range of conditions they can tolerate is rather
wide, and the similarity of the end products surprisingly complete.
In animals, one can usually distinguish 4 stages of embryonic development.
• Cleavage
Mitosis and cytokinesis of the zygote, an unusually large cell, produces an increasing
number of smaller cells, each with an exact copy of the genome present in the zygote.
However, the genes of the zygote are not expressed at first. The early activities of
cleavage are controlled by the mother's genome; that is, by mRNAs and proteins she
deposited in the unfertilized egg. In humans, the switch-over occurs after 4–8 cells have
been produced; in frogs not until thousands of cells have been produced. Cleavage ends
with the formation of a blastula.
• Patterning
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During this phase, the cells produced by cleavage organize themselves in layers and
masses, a process called gastrulation. The pattern of the future animal appears:
• front to rear (the anterior-posterior axis)
• back side and belly side (its dorsal-ventral axis)• left and right sides.
Gastrulation forms three major "germ layers": ectoderm, mesoderm, and endoderm. By
gastrulation, the genes of the zygote genome are being expressed.
• Differentiation
In time, the cells of the embryo differentiate to form the specialized structures and
functions that they will have in the adult. They form neurons, blood cells, skin cells,
muscle cells, etc., etc. These are organized into tissues, the tissues into organs, the
organs into systems.
• Growth
After all the systems are formed, most animals go through a period of growth. Growth
occurs by the formation of new cells and more extracellular matrix.
This paper also cover abnormalities that can occur during development often described
as congenital defects. There are many different ways that developmental abnormalities
can occur the 2 major types are Genetic (inherited) and Environmental (maternal)
derived abnormalities.
While genetic abnormalites will have well-defined impacts upon development,
maternally derived effects can be harder to define and variable depending on many
different factors (timing, exposure level, and combination with many other factors). In
addition, these two major causes can also interact giving a broad spectrum of both
major and minor abnormalities.
Genetic Abnormalities
Embryos with major genetic abnormalities, that impact on developmental processes, in
general fail to develop and are spontaneously aborted.
Many genetic developmental abnormalities involve only small DNA mutations
affecting individual or a few genes, exceptions to this are those that involve abnormal
segregation of chromosomes generating an abnormal chromosome number (complement) to the developing embryo.
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The most common trisomy (the number indicates the affected chromosome) is Down
syndrome (or trisomy 21) followed by Edwards syndrome (or trisomy 18) there are also
less common trisomy of chromosomes 9, 13, 15.
Importantly, the occurrence of these chromosomal abnormalities increases significantly
with increasing maternal age and requires increased prenatal testing.
Environmental Abnormalities
Environmental abnormalities (often called maternal derived) relate to lifestyle,
infection, maternal health and nutrition. In general, the more complex and the longer
time course of development, the more sensitive the system is to these abnormalities.
Infections of all kinds viral, bacterial and protist collectively grouped under the
acronym TORCH, which stands for: T oxoplasmosis, O ther organisms (parvovirus,
HIV, Epstein-Barr, herpes 6 and 8, varicella, syphilis, enterovirus) , Rubella,
Cytomegalovirus and Hepatitis. Infections (as well as other environmental conditions)
can also lead to increases in maternal core body temperature, Maternal Hyperthermia,
which has also been shown in animal models to be a potent teratogen.
Maternal drugs fall into many different classes and there is specific information for
each of these groups. Importantly the developing fetus is exposed to different levels andand metabolises more slowly all drugs. Lifestyle - alcohol (fetal alcohol syndrome),
smoking, and illegal drugs (Cannabis/Marijuana, Methamphetamine, Cocaine, Heroin,
Lysergic Acid Diethylamide) Maternal conditions - prescription drugs (therapeutic
chemicals/agents, thalidomide limb development) and non-prescription drugs (herbal).
Environment, for example smoking, chemical, heavy metals. Other maternal maternal
effects include changes in endocrine function (maternal diabetes, thyroid development).
A embryonic period
B fetal period
0-3 Death of the embryo
is possible
3-8 Susceptibility to
abnormalities isincreased
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8-38 Functional disorders are more likely
Figure 1: The incidence of congenital abnormalities as a function of time
* Teratogenesis
Teratogenesis is a prenatal toxicity characterized by structural or functional defects in
the developing embryo or fetus. It also includes intrauterine growth retardation, death
of the embryo or fetus, and transplacental carcinogenesis (in which chemical exposure
of the mother initiates cancer development in the embryo or fetus, resulting in cancer in
the progeny after birth).
A review published in 2010 identified 6 main teratogenic mechanisms associated with
medication use: folate antagonism, neural crest cell disruption, endocrine disruption,
oxidative stress, vascular disruption and specific receptor- or enzyme-mediated
teratogenesis.
Wilson's 6 principles
Along with this new awareness of the in utero vulnerability of the developing
mammalian embryo came the development and refinement of The Six Principles of
Teratology which are still applied today. These principles of teratology were put forth
by Jim Wilson in 1959 and in his monograph Environment and Birth Defects. These
principles guide the study and understanding of teratogenic agents and their effects on
developing organisms:
1. Susceptibility to teratogenesis depends on the genotype of the conceptus and the
manner in which this interacts with adverse environmental factors.
2. Susceptibility to teratogenesis varies with the developmental stage at the time of
exposure to an adverse influence. There are critical periods of susceptibility toagents and organ systems affected by these agents.
3. Teratogenic agents act in specific ways on developing cells and tissues to
initiate sequences of abnormal developmental events.
4. The access of adverse influences to developing tissues depends on the nature of
the influence. Several factors affect the ability of a teratogen to contact a
developing conceptus, such as the nature of the agent itself, route and degree of
maternal exposure, rate of placental transfer and systemic absorption, and
composition of the maternal and embryonic/fetal genotypes.
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5. There are four manifestations of deviant development (Death, Malformation,
Growth Retardation and Functional Defect).
6. Manifestations of deviant development increase in frequency and degree as
dosage increases from the No Observable Adverse Effect Level (NOAEL) to a
dose producing 100% Lethality (LD100).
In Teratogenesis can be grouped into several kind, according to the cause include:
1. Twin attached
Attached a light twin-called Siamese twins while severe twin-called monster double or
duplex.
Twins attached from 2 possibilities.
1. Not perfect left-right primitive streake cleavage 2. Imperfect seed layer splitting
Example twin attached:
• Tthoracopagus (chest knit). • Eraniopagus (head knit). • Phygopagus (hip knit)
2. Teratoma. Tumor-containing tissue derivet (three layers seed).
3. Physical Disabilities at Birth
• Lack of fingers and toes etc.. • Lack of organs pital.
4. Teratology. Disability occurs because:
- Impaired growth of buds of a tool - Growth stopped in the middle of the road
- Excess growth - One direction of differentiation
The photo on the left shows the tadpole that developed from a frog embryo that had
been injected with mRNA for activin. At the 32-cell stage of cleavage, a single cell —
that would normally have gone on to form part of the belly of the animal — was
injected with activin mRNA. A two-headed tadpole resulted (arrow). (A normal tadpole
is shown on the right for comparison.)
Figure 2: normal vs. abnormal frog embryo
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Figure 3: Teratogenic effects Figure 4: abnormality development in human embryo
of chemicals show up early and
readily in transparent tadpoles.
Teratogenic agents
A wide range of different chemicals and environmental factors are suspected or are
known to be teratogenic in humans and in animals. A selected few include:
• Drugs and medications: tobacco, caffeine, drinking alcohol (ethanol) (see fetal
alcohol spectrum disorder ), isotretinoin (13-cis-retinoic acid, Roaccutane),
temazepam (Restoril; Normisson), nitrazepam (Mogadon), nimetazepam
(Ermin), aminopterin or methotrexate, androgenic hormones, busulfan,
captopril, enalapril, coumarin, cyclophosphamide, diethylstilbestrol, phenytoin
(diphenylhydantoin, Dilantin, Epanutin), etretinate, lithium, methimazole, penicillamine, tetracyclines, thalidomide, trimethadione, methoxyethyl ethers,
Flusilazole, valproic acid, and many more.
• Environmental chemicals: polychlorinated biphenyls (PCBs), polychlorinated
dibenzodioxins a.k.a dioxin, polychlorinated dibenzofurans (PCDFs),
hexachlorobenzene hexachlorophene, organic mercury, ethidium bromide, etc.
• Ionizing radiation: atomic weapons fallout (Iodine-131, uranium), background
radiation, diagnostic x-rays, radiation therapy
• Infections: cytomegalovirus, herpes virus, parvovirus B19, rubella virus
(German measles), syphilis, toxoplasmosis, Venezuelan equine encephalitis
virus. (An easy way to remember maternal infections is TORCH:
Toxoplasmosis, Other agents, Rubella, CMV and HSV.• Metabolic imbalance: alcoholism, endemic cretinism, diabetes, folic acid
deficiency, iodine deficiency, hyperthermia, phenylketonuria, rheumatic disease
and congenital heart block , virilizing tumors.
Table 1: Some examples of teratogens known to cause human malformations
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CONCLUSION
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* If a number of fertilized eggs of a given species are provided with conditions that
enable them to develop at all, they will.
* It is possible, of course, to produce abnormal organisms by submitting a developing
system to stimuli not usually encountered in a normal environment, such as certain
chemicals.
* A congenital malformation is an anatomical or structural abnormality present at birth.
Congenital malformations may be caused by genetic factors or environmental insults or
a combination of the two that occur during prenatal development.
* A teratogen is any agent that causes an abnormality following fetal exposure during
pregnancy.
* Teratogens are known to affect the development at the embryonic stage.
REFERENCES
http://www.columbia.edu/itc/hs/medical/humandev/2004/Chpt23-Teratogens.pdf
http://www.informatics.jax.org/greenbook/chapters/chapter14.shtml
http://www.mindfully.org/Pesticide/Teratogens.htm
http://www.ncbi.nlm.nih.gov/books/NBK9998/http://www.purdue.edu/rem/ih/terat.htm
terat.htm