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NST110_fa04mt1 - I.D ’S‘i Zuni-Wing am Name l< fi-vl...

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Unformatted text preview: I.D,# ’S‘i Zuni-Wing am Name l< fi-vl ”\ University of California, Berkeley Department of Nutritional Sciences and Toxicology Toxicology Exam #1 (12 pts) 1. Briefly define the following terms as they are used in this course: LB0409ch5 M! Si N NST 110, Fall 2004 a. Hormesis ‘ mm l-xwwi ca 1R. 1 ( L ‘x -1 . “a \m o... h V“ <1. {—fi NJ l fl" ( ngy‘ofigfi. _ & r« In din! dilfifi ( 1: w (fi_1w'3r (o :R Ligfl _ ,, 011w, CY”. -' 1. ft.) ‘9“- L‘kfifkm‘. n "i i. b. NIH Shifl 1""&"i0-li:3\'>1.-1":'. a CL?“ * ~J . k A “A L g . . b <71». 1,1,“ 11,. 1 . «= c t m c 1.1.. 11.. I; "‘17 --——x7 gum 52—: —R 01.3.1.1“ .( x.- 1.3.41 E. _ H? >3. -. , . - 1., W” e. Cohort study -. any, a Q 1- _‘ 1 r t a,» _ a .; r > '_ {‘1 mm) 4, 1‘5} (3“ a S( Q m». ' {‘ A." ‘- d " 6.. \3 ”‘5‘”? IM 3 .1 ‘ ’ i 31'” (LLB/~23 Q1 '1 Kit; "rm. i '_ 4;: ‘x ’ "- 5' 1. 1. g 3;, {:i j, ~r._-_~,. "{"n “W; m 1‘ r) (10 pts.) 2. Substances A and B have identical response curves for one type of activity with 1% response dose = 0.8 microgram/ kilogram (ug/kg) and 99% response dose 1 2 ug/kg. They also exhibit the same 30% response dose at 90 ng/kg. They have 50% reSponse doses of 100 ug/kg (A) and 1000 ug/kg (B). a. Draw/curves for effective and toxic responses for substances A and B L; 2.11 {gr} U 1937‘... that (Eff): ,1" TD , ‘ L T. .k\ 1;» . ‘w %\ in (371 :— 9--~-e---~1—r—v:\ - 1 1 . 99.0..) (in a, L t. in"! b. Estlmate the NOAELs for A and B. ; fl. 3 D f '1. :~..».ao\:‘—i #1 A x .}~%9\ eel-Jew» “1'10 A““<h“t1k c. What are the approximate margins of safety for A and B? Lflmi’cmit-r {43' :4. 2mm“ - *7 n1 ”es-.71 :fi’ -; {rm i5. '1; f‘ 1 7 1 r _ mourn H. 5km Them than DE % _ L A0 ’ 5 1/ ' i 6. Which substance is safer? Briefly explain. fl Ac media. was 1- we" a. a. {gt—«.3 1, A _; 5. ,1". r ( {we w». Q. 1.; ' p TM QLJQ (XL (‘ j, .23; C? '5’ :3 M 41;: C3 «44 3 KY. \ €\L KL!» 0’? ( {ch-.341 V up ”,3 1L&(c\>g_( do? 1-. mi, j. a z-irw 1 TD 3?, , 1.: O( mgW—N kwr‘efif chm :c . ‘ ‘ a 1 % '13 S a 5’5 / €31; ow-.,.,-§ 1-1:.“ «Zn-“‘32? .13; . mn- wait 13 “— M? B “ti“‘fi'i': (. Wk (*8 W. 4L". - J2“- '. ‘r’l‘w. tknni 1 S, me: o b ‘le who). @vd‘Iu ‘A. “fig-{Ari . TH“ ‘5 ‘° 5 .fl_\ E3 at. " ”3!- »ei- '5: :1 "-"'F-: bafiit‘i ‘3 01.41 so M {-(r';;".} em 3...»; 8'1 icflxfi - b\ o“: r Cw s Lawn—V am“: 7,, .33; y. gm 0‘19} . < y r. Ly «E w?— R ‘bfs '- mgmfgag {L233 ‘94 ga- Lv" - C} i; a- 335;“ -f . :. 5.5 :57 cw 3 -v_- 5.5., (6 pts) 4. How can storage affect to toxicity of a substance. Provide two possible examples. T‘s—tr 0, mew»! {at ‘A‘1 o x\ 6.1% Go“! 1 lmwxw 3-1:: (' 6.3.232. 5* T is. > L ‘3 nut-Arm 6» ii? c»'\.: ‘=' - " '- <1. // yang lei-a1". L a: V629!» 9-» 4:3 H‘N "gr-m. . "TO K. Lin-.4 Me. ...i {,3 he: <5 4‘ gt; 8-? 5 "l A \"g' L( r—w 0.2:: (1.4:; .4 L, Wafer?! L r‘l‘\ Dani hi (3.; To Ps‘w giant “‘3‘. ’1‘1r-a n, *3 In. 51-.“ {45-1. i... 3 a. 3 Lang-- ‘ l i, a .51 K;- t (3 -. W . __, "5*- W3 X.» . E I.» L- , WOJ d do. or a. a- w. _ (6 pts.) 5. Briefly explain how a high respiration rate might affect the toxicity of a certain group of substances. - {3). ‘n\ Sim. ( L3G“ r e513 on ( (aft (1... . Umbekd “re“ ’3‘ '15”; i a 3~"_:_-"‘V"C‘I 3‘ ‘~ "5‘ (up: M a S“ ‘5 Y wk: (“A—x NHL-vi caning-u :4:- (Z-f‘s} ‘2 "F“ "“3" "53% I'm T. * t"- 6 TM ‘00 CH4. 0» 3 Mo cL ms .4 3mm ‘MW 3 . {2; at". L .2331- a... a”; 2. “~0va 91 ‘ok Me. (a. 4 he“?!- ‘s M1 [x U L71 La in». 14mg“ wcflrme‘m '5 m3, , vfi 5 “b'gflr 64" KJL 3 9-377 bfi-S‘t is: QI’DQU’V {.73 axes-c)- Lei {a mgr 5 ~55.) i, ‘flli-ak. . {w (8) 6. Briefly explain why carcinogens in particulate matter in the air can cause lung cancer even though very little of the carcinogens is absorbed by- the normal lung. Cite two reasons. .y M V ' W.- a- MD ’1‘; mime. that“ w r?- "1"“ .g.‘ {,i, ,1 rv" «15.; ‘3’ ” ‘ - .. . | 7 i f ( “i3 (3 9 Q 215m arr-«a. m w «w s?- S r»: 2 ~» ’M e» a \ Viv-xv.“ (Ashe \ arm UL ( MM 6531 (”WWW 3 ( irvxmm 5,1 (30¢ rL—z, tun?) .t 3 (Kari . r ,. s «‘2 TM 7 ._ ,, __ {3.3.3 arr-Jib, :. 5% iii; .13”),ch a" . lil‘kL 47R Throw"! _ D ID# is’ql‘z‘lflafol": Name Raf-m. “5’s 1:. '(7 pts) 3. Provide a brief rationale for why we would expect to see a NOAEL for all substances. Give examples of the processes involved. (6) 7. How does methylmercury very efficiently penetrate the blood-brain barrier? Hm- RE l mu can»! u g a. m : kid 51‘ err Cm“; QMZ-‘utt tWi "the Hm - aw ems apart” 5.: as m 1 (1 TR“. #2: t 0‘3 d — van; 9 «a. ‘<’> LN (”u-c . TLL (moi c. ‘1‘..sz Ewe-ma} ii In: a, in.“ sin: Elk-e ilk; SJOS‘I ‘1‘“ L‘— Qg-\ n}. \ 3 a;‘,..jg,m_ e: {:1 I x. U. i '4 ‘L ”5“;- §2 '3 \— TL-f'} , LB0409ch 5 ID # Name K €_.V‘.{"\ Watt... (8) 8. Lipophilic substances are in general a much more hazardous class of chronic toxins than are hydrophilic substances. a. Explain briefly why this is so. L ‘lve ‘9 K it i. a~.,=e-ss5er~nt,s 3 cm put-«Latte. “P“ d ‘r t \ ‘0‘ a” t" ‘3 “’1‘ $15“”‘ 3 fl- 9" 3 a “f .7 &\ 3 c9 ”thin-‘5 (3..” 9‘1 19‘— 653‘5‘:er A 33"”, ‘Mf 7m {1 or? r H ”l {he 33% V a,“ $15.93*: on u. 3 act, rho: L. < Lane“ ‘51 be cc e'E and. w b. What biological processes are in place in the normal mammal to reduce the toxicity oflipophilic toxics? Cite three. a“; E g}. g T,“ V _ wmvif ’Q 1‘ '43 p—Vw‘ ctr.) C; ’I\ 3 l x L, '5, ”Ms ‘2': 41L ask a % to ’tce»=$,€‘mre~~< mil 6 war {7? R my” 3 1 ""5" 7 g "Y Q( cs}; .1 t’ ‘1 ck»... Cs, 'fi’ 33:321.- ‘. \le , {g xclflgfl'fi" Gf‘k' m LU mi mogul flmox'tm (10) 9. The following questions relate to the phase II metabolism of phenolic substances. a. What are the two most common phase II metabolites of phenolic substances and how does substrate concentration affect to levels ofproducts‘? as I , , " . 0." vs 5. 3 ‘ 2;)!“ CAL: (fir-v: EL “in: MW. 3; an“? ’3 A} , L U“: f! '3'; "‘ ’~" ii'f-‘vi ,9» 1% s‘vmx LoaUu "“2; V“ ‘ V k . .. unit l ELM: p—J; 35"“. La ( Q (“1“. (3.1} \ V‘Jfi' 12. to ma be» . {firvshtt‘ cw'fi'is'Ba-as; we; r rat: b.’ Which of these two classes of metabolites is more efficiently excreted in the "“ ‘ \ urine? Briefly explain. I— '/© 0' {ma-(£1 at KL”? .1 M- ‘C’i'i "*f E Fri/mi 5 LC} E?» +h- 9“ rm; (“w-51.. 3;»? .t‘ F1 "; f r ' [Li (1295?“ tr .f‘ _, ”:1 ’~'_ 1 . . go A 3;, 0. Which type of conjugate in more readily excreted Via the feces following entry - into the bile? Briefly explain. ' ' SS. 1 {1:3 f.“ g f t 6. . r 7. 1g, “4% ., “A 5.1 E ’3an L1 C F..o{_:'r£e L»: CC Q.“‘I‘ \ C) m flan » ‘ A. . a , . ;.. 1' ‘ v 1 a. T he. Q r e” t 1; lac. rte/1L a. Lav/K at H ': , ., a D 'e- m . (6) 10. The GSTs serve a fundamentally different purpose in xenobiotic metabolism than do the GT5 and STs. What is this purpose? Briefly explain. 5:9 :37 1 or» L“ $903 '7: an. EA Us? 5 2‘) if; Lac-1 Q. .5 Omci N C if“ V G533 v“ cJX X (“m 5;: x i '1 tr J; i r ~ ' 'fi V» : ~ . s 5-“ em" ’3 E: I "\ CLJ‘ k 3 F TF‘LV‘C ’3‘ "7“ I (” CM‘M‘.“ fibres, é in,“ \\ oar-s a; new an! (em? “43,1 3:; Mill's. at éw-efi-‘m aWL {354 . .4 .1 -, 7- 1-: c 7 , e x ago by ext (.3 (6) 11. Provide a short answer exam question and answer relating to the material presented thus far in the course. 14 b Lu ”ASE-1 2rd it‘- 1: kit? 0341’ a C.» 5 {AA 0,951 fir.‘ @ C 0‘, (mart bv‘cm's 1 '. .4 I) 1 me. \e\ war”. t ‘oi it; _~,vt'v<-~ q no :3 arm :3 51:, when? ‘ J m w G.‘.\ ‘4‘ hex {sf {3 "- ~55 .3; o g {A ( ‘30 my :xr'x o g g- r 3 Wm 0— r-w. Querzwx e", tn as ‘02.. {JD was» 41;. 5" Was: 02.x #42:; Cox (:1 ( n, arena, 3 -t but; ‘k U VAC—C s F a $3 5‘5: 5 .1 C "“59 ("5: roo- 01‘? “Wee-Cg" . W "‘9'“; 5“ «(was 21."; A» . .Hfl‘fl a“: \ $ROU)‘ mm. ”col, 3. «.L c: a. arr—ems {but “4‘ l rims, T.\ i f. MA 4:, = ’; sad. {Rx—r ask-£3” q oats :5 :1, r‘ L.) LBO409eh5 21.1., \ cs Lr't‘v vf. (1‘3 raw-[$38. G: a ’?f“.g’$.§e, r (S lea, (wk?- vi , \f e." ‘ ‘- " *' W . ‘o u, ttr’ Ex C6031 >13 r“: _ ID # I Name K a; It” Lion (15) 12. Suppose that compound X is a potent colon carcinogen when administered oraily but shows little toxicity when administered by intrave ous injection. 7 ii ; was N o L.--- ‘7 \_<'“§f / "’K'" ' _ OCH3 ) £134.54" {ET-i a. Indicate five (5) likely phase I metabolites of compound X and the enzymes that would mediate the reactions. (Indi e partial structures of the metabolites on the figure.) (3/ b. Indicate a likely metabolic activatio sequence involving a phase II process that Would account for the route-dependent carcinogenic activity of this compound. a . G M . PS ‘ x ._ V» A m. r} '; UN N h“ {'- L'N/Viv‘t ”1:11”;K é) “““"‘“—W W Q/ ‘\‘/r-’“w33:/3 we c l l o MAL 0. Indicate two (different) types of phase II products that would account for the low ip g toxicity of the substance. LBO409ch5 Kevin Yee October 12, 2004 Nutritional Science 110 Midterm 1 Corrections 1. a) hormesis: the theory that some toxic substances exhibit beneficial effects at low doses but at higher doses produce negative effects. A sample toxin that may follow this , behavior is radioactive exposure The graph will follow a U—shaped curve that dips below the threshold for adverse response at some point and enter a region of homeostasis, then later return above the threshold to exhibit a negative response. (3) cohort study: cohort studies evaluate individuais selected on the basis of their exposure to an agent under study. Based on exposure status, these individuals are monitored for _, ’ development of disease. They are studied over time to observe the rates at which diseases are developed. Often, demographics will be compared and used to segment groups. Article: J Gerontol (2004). Aging intervention, prevention, and therapy through hormesis. A Biol Sci Med Sci July 2004, 59(7):705-—9. Horrnesis may be represented by mild stresses on cells and biological pathways in revealing a beneficial response. The article describes such stresses such as pro-oxidants, aldehydes, irradiation, and heat shock. The study is not fully fleshed out in regards to entire molecular mechanisms; future research is required to determine its effectiveness in preventing diseases that are contracted due to old age, and in order to reduce the severity of such diseases. .\ ‘\ Z! . 2. a) (see attached) b) NOAEL of A is approximately (slightly less than) the TDl of A. It is difiicult to exactly calculate the TDl given the lack of information on the TD curve, but we can ,: certainly suppose it to be in the range between 2 and 90 ug/kg Given the sharp rise of 7 toxic response between 90 and 100ug, if we estimate the slope to be constant throughout the entire TD curve (m = (50—30)/(100—90) = 2), the TDI of A is approximately 71$ kEfrem the equation y : 2x - 150). 7— Another fair estimate of the NOAEL is the TDIO, which occurs at approximately a dose of 80 ug/kg, by the same equation. Likewise, the NOAEL of B islapproximately the T01 of B. Again, we can estimate the range to be in between 2and90 rig/kg Given the suspicious curve of the graph, we cannot assume the slope is constant throughout the whole curve, so we estimate the TDi to be the ED99 of the substance at Zugfkg. Using the slope of the curve would give us a negative dose as a supposed TDl or even TDIO. c) If the margin of safety for a substance is defined as LDl/EQQQ, I‘We do not have enough " information on the curve to presume anything about theJBB-rflesponse curve. Given the shape of the B curve compared to the A curve, however, we can assume that the LDl of B will be greater than the LDI of A, which means that the margin of safety for Berlin be greater than that of A, since their EDS are the same. This means that 13,333 a larger‘ margin of safety than A. a d) By comparing graphs, 3.3%afenbecause it takes a larger dose to obtain a comparatively higher toxic response than A. Because A is clearly more potent, B is logically safer due to the slower rate at which the graph rises. Article: Leopold A, Wilson S, Weaver JS, Moursi AM (2002). Pharmacokinetics of iidocaine delivered from a transmucosal patch in children, Anesth Prog, 2002 Summer; 49(3):82—7. This article describes the effects of a study conducted in order to determine the effectiveness of the DentiPatch lidocaine transoral delivery system, a transmucosal patch produced by Noven Pharmaceuticals, in providing a mild anesthesia for adults and children. In adults, Dentipatch application produces low plasma concentrations of lidocaine, this study was conducted to see what levels were produced in children and whether that level was safe or not. Blood samples were compared before and after application in a test group of eleven children between the ages of two and seven. The results were plotted and compared using dose—response graphs. As a result, toxic levels in children were not reached in this study, but the effects on adults were high enough to consider administering a warning nonetheless when the patch was applied to children 3. NOAEL is defined as the level at which there are no adverse effects exhibited upon exposure to a substance. Effects may be detected, but they are not adverse. This is possible because of the fundamentals of toxicology: dosage determines t0xicity. Therefore, for all toxins, there must be some (possibly hypothetical) level at which the subject experiences no adverse effects. Tests would be conducted and the vague points at which toxicity is observed in 1-10% of the test subjects would be considered the NOAEL if there is no specific one point. The TDlO value would be used if the curve did not dip . , ._ , l we! Q below that pornt, 1,3 M 3.5 3., ML an L swim-u. 3 Article: Ahmad SK, Brinch DS, Friis EP, Pedersen PB (2004). Toxicological studies on Lactose Oxidase from Microdochinm nivale expressed in Fusarinm venenatum. Regul Toxicol Pharmacol 2004 Jun, 39(3):256-70. This article refers to a series of tests pertaining to lactose oxidase and its effectiveness in oxidizing lactose onto lactobionic acid. NOAEL data are used in determining the level at which the enzyme was not observed to have any adverse effects in rats. After this study, the enzyme was tested on cultured human lymphocytes. The safety margin for exposure was determined to be adequate enough to be safe enough for use in the food industry. 6. Carcinogens may be absorbed along the pathway to the lung. For example, they may become trapped and absorbed through the mucous membrane in the throat area, then drawn the lung. Also, while they may not be immediately absorbed by the lung, particulate carcinogens may be stored in the area and disrupt normal functions thusly. Toxicity can occur at a storage cite, Their presence may be enough to create cancerous growths, given enough time. a” .~ "viii“fi " Article: Repacc J (2004). Respirable particles and carcinogens in the air of Delaware hospitality venues before and after a smoking ban. J Occup Environ Med 2004 Sep, 46(9):887-905. A study is in place to determine whether the supposed reduction of indoor air pollutants actually lower the rate of respiratory cancer afler a law banning workplace smoke. Respirable particles are measured in casinos and bars; tests are performed to determine the increases in air quality before and after the law. The study is still in progress and does not have any direct conclusions thus far. 7. Methylmercury combines with cysteine, forming a structure similar to methionine, and the complex is accepted by the large neutrai amino acid carrier of the capillary endothelial cells. Essentially, methyimercury is toxic in humans because it enters the central nervous system thanks to carrier—mediated processes, allowing for prompt and efficient absorption. Article: Burger J, Gochfeld M (2004). Mercury in canned tuna: white versus light and temporal variation. Environ Res 2004 Nov, 96(3):23 9-49. This particular study was conducted to determine the concentration of mercury in canned tuna as opposed to mercury concentrations in wild fish, a property for which there generaliy exists far more data. (This statistic may be due in part to the tuna industry’s lobbying.) Tuna is the most popular consumed fish in the United States, which makes this study particularly relevant in the field of applied toxicology. This paper examines mercury concentrations in canned tuna obtained in a grocery store from 1998 to 2003, comparing the data with itself and with the FDA’s previous data. Methylmercury is an organic mercury; inorganic mercury was undetectable. The results of the study found that mean levels of mercury in white tuna were nearly three times as much as that in light or chunk tuna. The mean level in white tuna did not exceed the FDA recommended level of .5 ppm, but individual cans often exceeded that level. Data suggest that the levels have increased slightly since 1991, with the highest concentrations in the year 2001. Draining the can did not have any significant effects on mercury concentration. The paper concludes that these foodstuffs must be more frequently monitored in order to reduce their potentially toxic effects on the general population, given the potential damage that may be wrought by methylrnercury absorption. 9. b)/Glucuronidation occurs when UDP-glucuronic acid replaces the -OH group of a phenol. In becoming glucuronidated, the molecule becomes more soluble and less lipophilic, and thus readily excreted via the urine. c) Sulfonatignwguccurs with the addition of a PAPS group replacing the -OH of the phenol. , Sulfonated products tend to be excreted Via the bile. Once in the intestine, they will either be excreted through the iéééé'hiiéafisorbed if the conjugate becomes hydrolyzed. Upon reabsorption, since there is a low concentration, the molecule will likely become sulfonated again and excreted via the bile. Eventually the molecule will not be reabsorbed due to its loss of lipophilicity and thus become excreted in the feces. Micle: Mesia—Vela S, Kauffman FC (2003). Inhibition of rat liver sulfotransferases SULTlAl and SULTZAl and glucuronosyltransferase by dietary flavonoids. Xenobt'otica 2003 Dec, 33(12):1211-20. In this study, dietary flavonoids were tested on their ability to alter the conjugation of oestradiol by sulfotransferases and glucuronosyltransferases present in rat livers. All flavonids inhibited the sulfonation of oestradiol by STs and GSTs, though at different levels for each flavonoid and each particular enzyme. The conclusions of the study present that some STs are much more sensitive to inhibition by flavonoids than others, suggesting a dependency on the number and position of hydroxyl radicals in the flavonoid molecule. 12. a), b) (see attached) Article: Malaplate-Armand C, Leininger—Muller B, Batt AM (2004). Astrocytic cytochromes p450: an enzyme subfamily critical for brain metabolism and neuroprotection. Rev Neurol (Paris) 2004 Jul, 160(6-7):651-8. The article describes the effectiveness of Cytochromes P450 as expressed in astrocytesi which are involved in multiple brain functions, in neurornetabolic processes and neuroprotection. Astsroglial cells exhibit a larger level of CYP than in other areas of the brain, suggesting great importance in metabolizing psychoactive or lipophilic xenobiotics. A series of tests were performed to determine their effectiveness in the laboratory. The paper concludes that greater research involving astrOCytes is required to better understand neuroprotective processes and reveal better therapeutic perspectives. (2. //,;)A"1_.. 71‘ {H01 “E ‘ ;(F;§ , Y; gay , ‘~ (" orig/”Tm“ ““42! ' 73mm.” ,___ MY" 7”” 0&4 b3 0 I H N_ Ma, Pa: \. | I: , ’41? 1:. x} get-*1». T? ‘i J - 3H ‘ 4,4“: , 5-410 ‘ fl : 'N . yr 2 r7143 #47 ‘2 K ‘ ‘w . 5v V a“ 9 EH \ '94“? on» La. :3 ijsNA we \ N02 ...
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