A+ Graded Paper
NUSCTX 11 Final Exam – Expert-Crafted
Q&A Set for Exam Excellence
Questions and Mark scheme
Version: Final
,How Do Endocrine Disruptors Work? - ✔✔Endocrine Disruptors: exogenous ("outside" chemicals that disrupt
the endocrine system by mimicking or blocking hormone actions
Alter Hormone Levels - hormones need to be well-regulated (potent in small amounts, regulated in counter-
regulatory or negative feedback loop systems); disruptors can interfere with regulatory systems
Bind to Receptors (Agonism) or Block Hormonal Action (Antagonism) - hormones are first messengers;
endocrine disruptors can bind to receptors and mimic hormone action (agonism) or the endocrine disruptor can
bind to hormone and block endogenous hormone binding (antagonism) - limited number of receptors (if body is
overwhelmed with endocrine disruptors, normal endogenous hormones are unable to bind)
Hormones Need to Mediate Signaling - endocrine disruptors an alter hormonal responses and steps in actions
that occur downstream after binding to receptor (disrupt hormone signaling)
Can cross the placenta barrier and potentially affect fetus (effects can linger longer after the child is born) -
trans-generational effect
Toxicants vs. Endocrine Disruptors - ✔✔Toxicants: response in a linear dose, response curve (dose is important
factor - able to predict response because it follows a pattern)
Endocrine Disruptor: dose-response curves are non-monotonic (not a linear curve), depending on type of
chemical can respond in varied ways that are difficult to predict; no clear threshold
Mechanism of Action for DDT - ✔✔Synthetic chemical, used as an insecticide (World War II - combat malaria
typhus, effective against malaria and other insect-borne human diseases); brought into wide agricultural and
commercial use (80 million pounds applied all over the world from the 1940s to 1960s); in the 1970s, people
began to have increased awareness of detrimental effects (usage declined due to insect resistance and
environmental and health concerns); 1972, DDT banned in the US because of harmful environmental impact
and potential hazard to human health
Silent Spring (Rachel Carson): increased mortality in birds due to application of the toxin; DDT implicated in
bio-concentration and biomagnification in food chains; raised political awareness; accused chemical industry of
spreading disinformation and public officials of accepting industry claims uncritically
Endocrine Disruptor: reproductive abnormality (body breaks it down, metabolizes compound into DDE, another
endocrine disruptor); long half-lives because they can accumulate in fat tissue, slowly released in body (long-
lingering effects); DDE is androgen receptor antagonist (blocks effect); rats tested with DDT have decreased
sperm number and motility, decreased testosterone production, and increased FSH and LH (hormones found in
biological females); DDT mimics estrogen; exposure to DDT leads to birds having thinner egg shells (higher
probability birds will not survive, reduction in enzyme key to shell formation)
Mechanism of Action for DES - ✔✔Disrupts estrogen, synthesized in 1938 and considered non-steroid - close
enough to mimic estrogen that it can bind to receptor; prescribed to pregnant women between 1940 and 1971 to
prevent miscarriage (common belief was that miscarriages were caused due to decreased estrogen levels - later
studies showed DES treatment increased risk of miscarriage because it mimicked the estrogen structure and
bound to receptor, displacing and outcompeting the body's natural estrogen)
, In 1971, DES was shown to cause a rare vaginal tumor in females exposed in-utero; tumors also caused in skin,
lung, liver, and uterine and other reproductive system tumors in female offspring of exposed women
DES mainly activates estrogen receptor-a and promotes abnormal proliferation of reproductive duct cells
DES Daughter/DES Son: effects of DES are trans-generational (can cross placental barrier - children experience
lingering effects, such as DES Daughters being more likely to experience early menopause)
Mechanism of Action for Atrazine - ✔✔Weed-killer used on corn for grassy and broad-leafed weeds, most
highly used in herbicides for corn and grain (inhibits photosynthesis); toxic effects came from observations in
frogs that lived around farms (male frogs eventually turn into female frogs after exposure at low ecologically
relevant doses)
Atrazine induces enzyme aromatase (converts testosterone into estradiol) - in Tyrone Hayes' study, he exposed
frogs to low levels of atrazine and found it was able to feminize male frogs (develop ovaries, had both ovaries
and testes - considered hermaphrodies)
Mechanism of Action for PCB - ✔✔Group of chemicals, synthetical chemical used for industrial purposes
(commonly found in power transformers and different capacitors); banned in late 1970s but still exists in
environment (highly lipophilic, difficult to remove)
Disrupts thyroid hormones (reduce the ability of thyroid hormones to bind to transport proteins, body cannot
bring thyroid hormone to receptor), inhibits conversion of T4 (inactive hormone) to T3 (active hormone), acts
as agonist or antagonist of thyroid receptor (eliminates chance for endogenous hormones to bind)
Mechanism of Action for STZ - ✔✔Identified in late-1950s, used as an antibiotic, selectively toxic to pancreatic
beta cells (discovered in 1960s - cells that produce insulin); able to reduce and disrupt insulin production and
act as an endocrine disruptor (enters through glucose transporter 2, type of transporter only expressed in
pancreatic beta cells)
It is only taken up by pancreatic beta cells and reduces insulin promotion - with high amounts, it destroys beta
cells, leading to no insulin int he body (causing Type I Diabetes), also causes DNA damage and kills cells
Mechanism of Action for BPA - ✔✔A monomer used in the production of a lot of different plastics (precursor
for flame retardants, used in a lot of different consumer products like reusable plastic bottles, glasses, toys,
thermal paper, etc.), can be slowly released from materials based on temperature, pH, overall wear and usage;
able to cross placental barrier
Exerts estrogen-like effects (bind to estrogen receptor and mimic endogenous actions of hormones); acts as
antagonist for androgen receptor (competes with androgen DHT), interferes with spermatogenesis, impairs male
reproductive function
Non-monotonic - higher responses in nanomolar range than in micromolar; ovrelap between obesogens and
endocrine disruptors (activate PPAR-gamma, master regulator of adipogenesis, disrupt thyroid hormone)
What Are The Steps of Carcinogenesis? - ✔✔Exposure to Carcinogen - body has repair systems to get rid of
initial mutations (must be exposed repeatedly, beyond the threshold of the body's repair system, or suddenly
exposed to a huge amount that overwhelms the body's threshold)
NUSCTX 11 Final Exam – Expert-Crafted
Q&A Set for Exam Excellence
Questions and Mark scheme
Version: Final
,How Do Endocrine Disruptors Work? - ✔✔Endocrine Disruptors: exogenous ("outside" chemicals that disrupt
the endocrine system by mimicking or blocking hormone actions
Alter Hormone Levels - hormones need to be well-regulated (potent in small amounts, regulated in counter-
regulatory or negative feedback loop systems); disruptors can interfere with regulatory systems
Bind to Receptors (Agonism) or Block Hormonal Action (Antagonism) - hormones are first messengers;
endocrine disruptors can bind to receptors and mimic hormone action (agonism) or the endocrine disruptor can
bind to hormone and block endogenous hormone binding (antagonism) - limited number of receptors (if body is
overwhelmed with endocrine disruptors, normal endogenous hormones are unable to bind)
Hormones Need to Mediate Signaling - endocrine disruptors an alter hormonal responses and steps in actions
that occur downstream after binding to receptor (disrupt hormone signaling)
Can cross the placenta barrier and potentially affect fetus (effects can linger longer after the child is born) -
trans-generational effect
Toxicants vs. Endocrine Disruptors - ✔✔Toxicants: response in a linear dose, response curve (dose is important
factor - able to predict response because it follows a pattern)
Endocrine Disruptor: dose-response curves are non-monotonic (not a linear curve), depending on type of
chemical can respond in varied ways that are difficult to predict; no clear threshold
Mechanism of Action for DDT - ✔✔Synthetic chemical, used as an insecticide (World War II - combat malaria
typhus, effective against malaria and other insect-borne human diseases); brought into wide agricultural and
commercial use (80 million pounds applied all over the world from the 1940s to 1960s); in the 1970s, people
began to have increased awareness of detrimental effects (usage declined due to insect resistance and
environmental and health concerns); 1972, DDT banned in the US because of harmful environmental impact
and potential hazard to human health
Silent Spring (Rachel Carson): increased mortality in birds due to application of the toxin; DDT implicated in
bio-concentration and biomagnification in food chains; raised political awareness; accused chemical industry of
spreading disinformation and public officials of accepting industry claims uncritically
Endocrine Disruptor: reproductive abnormality (body breaks it down, metabolizes compound into DDE, another
endocrine disruptor); long half-lives because they can accumulate in fat tissue, slowly released in body (long-
lingering effects); DDE is androgen receptor antagonist (blocks effect); rats tested with DDT have decreased
sperm number and motility, decreased testosterone production, and increased FSH and LH (hormones found in
biological females); DDT mimics estrogen; exposure to DDT leads to birds having thinner egg shells (higher
probability birds will not survive, reduction in enzyme key to shell formation)
Mechanism of Action for DES - ✔✔Disrupts estrogen, synthesized in 1938 and considered non-steroid - close
enough to mimic estrogen that it can bind to receptor; prescribed to pregnant women between 1940 and 1971 to
prevent miscarriage (common belief was that miscarriages were caused due to decreased estrogen levels - later
studies showed DES treatment increased risk of miscarriage because it mimicked the estrogen structure and
bound to receptor, displacing and outcompeting the body's natural estrogen)
, In 1971, DES was shown to cause a rare vaginal tumor in females exposed in-utero; tumors also caused in skin,
lung, liver, and uterine and other reproductive system tumors in female offspring of exposed women
DES mainly activates estrogen receptor-a and promotes abnormal proliferation of reproductive duct cells
DES Daughter/DES Son: effects of DES are trans-generational (can cross placental barrier - children experience
lingering effects, such as DES Daughters being more likely to experience early menopause)
Mechanism of Action for Atrazine - ✔✔Weed-killer used on corn for grassy and broad-leafed weeds, most
highly used in herbicides for corn and grain (inhibits photosynthesis); toxic effects came from observations in
frogs that lived around farms (male frogs eventually turn into female frogs after exposure at low ecologically
relevant doses)
Atrazine induces enzyme aromatase (converts testosterone into estradiol) - in Tyrone Hayes' study, he exposed
frogs to low levels of atrazine and found it was able to feminize male frogs (develop ovaries, had both ovaries
and testes - considered hermaphrodies)
Mechanism of Action for PCB - ✔✔Group of chemicals, synthetical chemical used for industrial purposes
(commonly found in power transformers and different capacitors); banned in late 1970s but still exists in
environment (highly lipophilic, difficult to remove)
Disrupts thyroid hormones (reduce the ability of thyroid hormones to bind to transport proteins, body cannot
bring thyroid hormone to receptor), inhibits conversion of T4 (inactive hormone) to T3 (active hormone), acts
as agonist or antagonist of thyroid receptor (eliminates chance for endogenous hormones to bind)
Mechanism of Action for STZ - ✔✔Identified in late-1950s, used as an antibiotic, selectively toxic to pancreatic
beta cells (discovered in 1960s - cells that produce insulin); able to reduce and disrupt insulin production and
act as an endocrine disruptor (enters through glucose transporter 2, type of transporter only expressed in
pancreatic beta cells)
It is only taken up by pancreatic beta cells and reduces insulin promotion - with high amounts, it destroys beta
cells, leading to no insulin int he body (causing Type I Diabetes), also causes DNA damage and kills cells
Mechanism of Action for BPA - ✔✔A monomer used in the production of a lot of different plastics (precursor
for flame retardants, used in a lot of different consumer products like reusable plastic bottles, glasses, toys,
thermal paper, etc.), can be slowly released from materials based on temperature, pH, overall wear and usage;
able to cross placental barrier
Exerts estrogen-like effects (bind to estrogen receptor and mimic endogenous actions of hormones); acts as
antagonist for androgen receptor (competes with androgen DHT), interferes with spermatogenesis, impairs male
reproductive function
Non-monotonic - higher responses in nanomolar range than in micromolar; ovrelap between obesogens and
endocrine disruptors (activate PPAR-gamma, master regulator of adipogenesis, disrupt thyroid hormone)
What Are The Steps of Carcinogenesis? - ✔✔Exposure to Carcinogen - body has repair systems to get rid of
initial mutations (must be exposed repeatedly, beyond the threshold of the body's repair system, or suddenly
exposed to a huge amount that overwhelms the body's threshold)
