I was wondering if anyone would interested in helping me answer a few questions concerning toxicology?
What an odd post! What sort of questions, then peeps will be able to tell you if they can answer them.
If it’s “what’s your poison?”, mine’s a large glass of Rioja, thanks for offering!
posting questions would help!
If you don’t want to, pm me I might be able to help.
Define, in layman’s terms, the median effective dose, and describe what it is useful
for. Compare the advantages and disadvantages of the traditional (e.g. Litchfield-
Wilcoxin) method of calculating the ED50 with the “up-down” methods (e.g.
Teflon has been in the news lately. A class action lawsuit alleges that DuPont
workers have been exposed to perfluorooctanoic acid (PFOA), the precursor
monomer that is used to make Teflon. Without getting into the merits of the suit,
why (i.e. the physical/chemical properties) is PFOA toxic, yet Teflon is so non-toxic
that it can be permanently implanted (e.g. artificial hips) in the body? (One sentence
ought to do it.)
Compare and contrast the practical differences (examples would be good) between
the concepts of “toxicity” and “hazard” as they were discussed in class. (Note:
different authors sometimes use different terms for the concept I called “hazard”. I’m
interested in what we talked about in class.)
How does a “classic” (i.e. data based) toxicokinetic model differ from a
physiologically based pharmaco(toxico)kinetic model? Describe the assumptions
underlying each and the relative advantages/disadvantages of each.
A) Describe an simple experiment to determine the apparent volume of distribution
(Vd) of gentamicin in any mammalian species. For simplicity, assume that you have
a gentamicin assay that is sensitive, cheap and easy. Furthermore, assume that
gentamicin is excreted unchanged. B) You determine that the Vd in the mouse is 2
liters. What does this tell you?
You’ve been assigned to a team to design a new insecticide to control mosquitos in
urban parks. Obviously, you want a compound that exhibits a high degree of
selective toxicity toward insects vs. mammals. List three possible
chemical/physical/physiological properties (there are many more) that might confer
such selectivity on your compound. (To keep it simple, only worry about the things
that might affect acute toxicity.)
You’ve been asked to evaluate the potential safety of a flame retardant for
spacesuits. Chronic topical administration near the LD50 (1000 mg/kg) resulted in
an increased incidence of skin tumors in rats, however none of the lower doses did.
High dose (1000 mg/kg) rats also showed a considerable degree of dermal necrosis.
Neither the Ames test nor any of the other in vitro tests of mutagenicity showed any
evidence of activity. What kind of carcinogen (genotoxic or epigenetic) is this? Do
we use this compound? Justify your answer.
Explain why cirrhosis due to chronic ethanol poisoning continues to get
progressively worse long after ethanol and its metabolites have been
eliminated from the organ.
Design a series (both in vivo and in vitro) of experiments to measure the
hepatotoxic potential of a new human drug. For the moment, assume that: 1)
price is not a serious concern; 2) the drug is a potential cancer
chemotherapeutic agent, i.e. it will only be used for fairly short periods of time
and in people who are likely to die without it, so we’re not terribly concerned
with latent chronic effects.
The mammalian kidney contains both organic anion and cation transport
systems in the proximal tubular epithelium. How might these systems
potentially influence the toxicity (or usefulness) of a drug like cephaloridine or
What is the significance of mean aerodynamic diameter in relation to
diseases such as bagassosis or byssinosis? In relation to hydrogen sulfide
toxicity? (Be careful… Trick question.)
Atypical bovine pulmonary emphysema & edema (ABPE) is a condition
associated with a sudden switch to high dietary tryptophan and ruminal
production of the pneumotoxin 3-methylindole. The latter compound exhibits
a range of organotropism in different mammalian species. For example, it
primarily affects the renal proximal tubule in the male mouse. Explain why
this might be so. (One paragraph only. I’m really more interested in
organotropism and species differences than ABPE, per se).
You’re working as the safety officer for a company that produces a variety of
plastics. The manufacturing process involves acrolein, phosgene and a
number of other nasty respiratory toxicants. Despite standard process
designs that minimize exposure, the company wants to monitor workers for
any incipient lung injury to head off problems before they get out of hand.
Devise a battery of non-invasive tests you could use to recognize early
pneumotoxic damage before it gets out of control. [Hint: we’re talking about
apparently healthy humans, so techniques that involve death of the subject
are off limits.]
Give two different general effects which a xenobiotic have on the immune
system. By “general” I’m referring to the fashion in which the system is
affected, not just three different examples of compounds which all cause the
same effect. (Dr. Belden discussed at least 3)
Summarize the evidence available to date for the toxicity of Vioxx. Was the
decision to remove the drug from the market justified from a toxicologic
standpoint? Defend your answer. [Note: Citations are important, but I’m
more interested in interpretation of the facts than a recitation of trivia, or
regurgitation of the arguments on the net.]
A student asked me Monday if eating a “package” of D-con (we’ll presume
the mouse size) would hurt his 1 year old Labrador pup. What do I tell him?
Defend your answer with numbers and provide alternatives for what to do if
you’re wrong. (This one is going to require some horse sense and maybe
even some non-library, non-internet research).
How might a weight loss drug (e.g. fen-phen) produce heart disease?
Please postulate a mechanism of action based up what we’ve discussed
throughout this Fall. (I’m not interested in epidemiologic associations or
clinical investigations. I want a plausible explanation for what could happen
at the cellular, organ and organismal levels.) You don’t have to give me a
“right” answer, but it has to be believable in terms of what is known about the
A patient complains of a bullous, erythematous, nonpruritic, discrete rash on
her forearms. An occupational history indicates that she works as a checker
at a supermarket and that several co-workers have had similar rashes.
Affected workers all came from the produce or floral sections or the check
out lanes where they were likely to have contact with fresh vegetables, e.g.
celery and fresh flowers. Meat and bakery employs haven’t had any
problems. Affected workers were also significantly more likely than
unaffected workers to have used a tanning salon during the last couple of
weeks. Suggest a (or more than one) possible etiology, pathogenesis and
describe what you’d recommend to correct the condition.
A pre-pharmacy student noticed that the active ingredient in her horse
wormer was the same as in the stuff she bought for her dog. The only
difference she could see was the price. She contacted the manufacturer and
(after a lot of phone calls) ascertained that the active ingredient in the dog
wormer came from the same production line and was chemically and
pharmacologically identical to the horse wormer. She calculated a canine
dose of the horse product, based upon the concentration of active ingredient,
and gave it to the Sheltie, which promptly started slobbering and convulsing.
What didn’t she consider?
Halothane is an inhalation anesthetic that used to be very commonly used in
both veterinary and human surgery. Its uptake via inhalation is best
described as “ventilation limited”. As with any drug (especially the
anesthetics), halothane is potentially very toxic, and has killed more than one
patient when overdosed. With nothing more than I’ve given you in this question,
and your extensive theoretical knowledge of dosimetry, how would you treat
We can use any source but he really only wants us to find this information on the web, like an internet research vocation.
Blime! I’m not surprised you didnt want to type all that lot out!
I’m not a toxicologist myself, more a zoologist, but here’s my attempt at a few of the questions.
(Warning - these may be wrong!)
2.the monomer may undergo a physical/chemical change when made into the final product.
- I see we’re doing your homework for you!!
5, physical such as presence of exoskeleton, method of breathing - both of which mean less is absorbed as fewer porous surface and mucus membranes
differences between dog and equine digestion. eg dogs a omnivore, horse is herbivore, physical differences in digestive systems.
flush out the lungs with lots of nice oxygen.
Hope this helps. If you succeed I want some of the credit, if you fail, you’re on your own buddy!
I have most done, I’ll post the answers when I finish. I noticed you only did the easy ones
I think I prefer MY question - and it’s still a large glass of Rioja!