Aging & Senescence

20 questions • 1 test • tap a section to begin

Welcome! Aging & Senescence — 20 questions across 1 tests.

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  • Test 1 (7.3) — Aging & Senescence

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7.3 Aging & Senescence — Test 1
Q1. The maximum number of times a normal human somatic cell divides before stopping is the:✓ Hayflick limit
Q2. Replicative senescence (the Hayflick limit) is mainly caused by:✓ Progressive shortening of telomeres with each division
Q3. Which does NOT promote aging in humans?✓ Activation of telomerase
Q4. Telomerase counteracts cellular aging by:✓ Adding repeats to telomere ends to maintain their length
Q5. Immortalization of mouse embryonic fibroblasts (bypassing the Hayflick limit) is most readily achieved by:✓ Transformation by overexpression of an oncogene
Q6. The free-radical (oxidative-stress) theory of aging proposes that aging results from:✓ Accumulated damage by reactive oxygen species over time
Q7. Cellular senescence is best described as a state in which a cell:✓ Permanently stops dividing but remains metabolically active
Q8. Senescent cells secrete inflammatory factors collectively called the:✓ Senescence-associated secretory phenotype (SASP)
Q9. Caloric (dietary) restriction has been shown in model organisms to:✓ Extend lifespan
Q10. Sirtuins, linked to longevity, are enzymes that act as:✓ NAD+-dependent protein deacetylases
Q11. Progeria (premature-aging syndromes) often result from defects in:✓ Nuclear envelope proteins (e.g. lamin A) or DNA-repair genes
Q12. The mitochondrial theory of aging emphasises that aging is driven partly by:✓ Accumulation of mitochondrial DNA damage and declining energy output
Q13. Why do most adult human somatic cells eventually senesce, while germ cells and stem cells can divide many more times?✓ Germ and stem cells express telomerase to maintain their telomeres
Q14. Senescence is considered a tumour-suppressor mechanism because it:✓ Stops potentially cancerous cells from dividing further
Q15. Apoptosis and senescence both contribute to aging and cancer prevention by:✓ Removing or arresting damaged cells
Q16. Aging at the organismal level is best described as:✓ A progressive decline in function and increased vulnerability over time
Q17. Accumulation of senescent cells with age is thought to contribute to aging because they:✓ Secrete inflammatory factors (SASP) that damage surrounding tissue
Q18. DNA-repair capacity is important in aging because:✓ Declining repair lets mutations and damage accumulate
Q19. Which best summarises the relationship between telomeres and cellular lifespan?✓ Telomeres shorten with each division, eventually limiting further division
Q20. Overall, aging is best understood as resulting from:✓ The combined effects of telomere loss, oxidative damage, declining repair and senescence