With suitable examples, compare genetic and induced teratogenesis.

Genetic Teratogenesis

Genetic teratogenesis arises from alterations in the genome of either the parents or the developing embryo. These alterations can be inherited mutations, de novo mutations, or chromosomal abnormalities. The effects are often complex and can involve multiple genes interacting with environmental factors.

• Mechanism: Mutations in genes crucial for developmental processes (e.g., Hox genes, signaling pathways) disrupt normal embryogenesis. Chromosomal abnormalities like trisomy (e.g., Down syndrome) lead to an imbalance in gene dosage.
• Causative Agents: Inherited single-gene disorders (e.g., cystic fibrosis, sickle cell anemia), chromosomal abnormalities, genomic imprinting defects.
• Timing of Exposure: The effect is present from conception, as the genetic defect is inherent in the gametes or arises during early cleavage stages.
• Examples:
  • Down Syndrome (Trisomy 21): Caused by an extra copy of chromosome 21, leading to intellectual disability, characteristic facial features, and congenital heart defects.
  • Cystic Fibrosis: An autosomal recessive disorder caused by mutations in the CFTR gene, affecting multiple organ systems.
  • Achondroplasia: A genetic disorder affecting bone growth, resulting in dwarfism.
• Predictability & Prevention: Genetic counseling and prenatal diagnosis (e.g., amniocentesis, chorionic villus sampling) can identify some genetic risks. Prevention is limited to avoiding reproduction if both parents are carriers of a recessive gene or if a chromosomal abnormality is identified.

Induced Teratogenesis

Induced teratogenesis results from exposure to exogenous (external) agents during critical periods of development. These agents, known as teratogens, can disrupt normal embryological processes, leading to congenital malformations.

• Mechanism: Teratogens interfere with specific developmental events, such as cell proliferation, cell migration, apoptosis, or differentiation. The mechanism of action varies depending on the teratogen.
• Causative Agents: Drugs (e.g., thalidomide, isotretinoin), infectious agents (e.g., rubella virus, Zika virus), environmental chemicals (e.g., mercury, PCBs), radiation, maternal conditions (e.g., diabetes, hyperthermia).
• Timing of Exposure: The timing of exposure is critical. Different organs and systems are vulnerable to teratogens during specific developmental windows (organogenesis).
• Examples:
  • Thalidomide: Exposure during weeks 3-6 of gestation caused severe limb defects (phocomelia).
  • Rubella Virus: Infection during the first trimester can lead to congenital rubella syndrome, including deafness, cataracts, and heart defects.
  • Fetal Alcohol Syndrome: Exposure to alcohol during pregnancy can cause facial abnormalities, growth retardation, and intellectual disability.
  • Zika Virus: Infection during pregnancy can cause microcephaly and other brain defects.
• Predictability & Prevention: The effects of some teratogens are well-established, allowing for preventative measures (e.g., avoiding certain medications during pregnancy, vaccination against rubella). However, the effects of many environmental chemicals are still being investigated.

Comparative Table

Feature	Genetic Teratogenesis	Induced Teratogenesis
Cause	Inherited or de novo genetic mutations/abnormalities	Exposure to exogenous teratogens
Timing of Effect	Present from conception	Dependent on the critical period of organogenesis
Predictability	Can be predicted through genetic testing (variable)	Predictable based on known teratogen effects and timing of exposure
Prevention	Genetic counseling, prenatal diagnosis, avoiding reproduction if high risk	Avoiding exposure to teratogens, vaccination, managing maternal health
Reversibility	Generally irreversible	Sometimes reversible if exposure is limited and occurs later in development