L7: Effects on Cells, Tissues & Organs

Question 1

Cytotoxicity

Answer 1

toxicity to cells, cell death or injury in tissue

Question 2

Necrosis

Answer 2

cell death from disease/injury, localized or diffuse,

- Externally driven by radiation, chemicals, viruses, etc.

Question 3

Apoptosis

Answer 3

programmed cell death

• Internally driven by either lack of nutrients or extensive DNA damage
• Externally driven by other cells when not needed anymore

Occurs at lower contaminant levels than necrosis
Also occurs normally (as part of anatomical development and natural cell replacement)
Apoptosis from contaminants distinct b/c removes compromised cells that might lead to dysfunction or cancer
Failure of normal apoptosis contributes to carcinogenesis

Question 4

Apoptosis Series of Steps

Answer 4

Starts w activation of proteases, caspase enzymes
Cell then undergoes changes in Ca2+, K+, and water fluxes
Cell’s chromatin condenses, DNA fragments, apoptotic bodies form

Question 5

Appearance for apoptotic cells

Answer 5

Cell detaches from adjacent cells
Shape become irregular
Can break into fragments

Question 6

Difference b/w Necrosis & Apoptosis

Answer 6

Apoptosis:
Viable cell–>cell shrinks, chromatin condenses–>budding–>apoptotic bodies phagozytosed; no inflammation

Necrosis:
Viable cell–>cell swells–>blebbing–>cellular and nuclear lysis causes inflammation

Question 7

Somatic risk

Answer 7

risk of adverse effects on organism from genetic damage to somatic cells (e.g. damage leading to cancer)

Question 8

Genetic risk

Answer 8

effects pass on to next generation b/c of heritable damage to DNA (e.g. damage to gametes leading to birth defect)

Question 9

4 ways damage occurs on gene/chromosome level

Answer 9

sister chromatid exchange, chromosomal aberration, micronuclei, aneuploidy

These changes provide evidence of mechanisms for mutations or cancer

Question 10

Hyperplasia

Answer 10

Normal cells can multiply and increase in tissues, increase tissue size

Question 11

Hyperplasia can be triggered by: (2)

Answer 11

Hormones (e.g. increases in breast tissues) – hormonal hyperplasia

Normal repair mechanisms – physiologic hyperplasia

Question 12

2 types of pathologic hyperplasia

Answer 12

1. Injury or irritation – excessive hyperplasia

2. Hereditary changes to cells – neoplastic hyperplasia (cells no longer respond to normal control mechanisms)

Question 13

2 types of neoplastic hyperplasia (mechanism for cancerous growth)

Answer 13

1. Benign neoplasia: grows slowly, does not invade neighbouring tissue
2. Malignant neoplasia: grows rapidly, invades other tissues
   - more life threatening, pieces dislodge and move via lymph or blood to other tissues (metastasis)

Question 14

Tumours

Answer 14

Presence used as biomarkers for environmental carcinogens
Often, incidence of cancer related to level of exposure
Include cancers of stomach, uterus, ovary, intestine, skin, liver

Question 15

Beluga Whales in St. Lawrence River

Answer 15

Initial study examined 263 stranded whales
From area high in PAHs and metals from aluminum smelter

• Have high P-450 enzymes
• Cause of death: Parasites (22%), Cancers (18%), Infections (17%)
• Cancers include intestinal, stomach, uterus, skin, ovarian, salivary gland, bladder

Question 16

What exposures are linked to cancers?

Answer 16

Contaminants

• Benzene, Ni, vinyl chloride, As
• PCBs, PAHs, etc.
• Radiation

Substances: Alcohol, cigarettes

Dust and fibres: Asbestos, silica, soot (PAHs)