natgillin/translations-raw huggingface dataset:
a 12-nucleotide segment of single-stranded DNA that exists at both ends of the bacteriophage lambda's double-stranded genome.
405–411.
a mutation in which one or more (sequential) nucleotides is lost by the genome.
Behav., 64:661–669.
Electroporation
Edwards, P.M., Parker, V.H.
the application of electric pulses to increase the permeability of cell membranes.
Pharmacol., 40:589–591.
Endogenous gene
Davis, M. (1984) The mammalian startle response.
a gene native to the genome.
Koch, M. (1999) The neurobiology of startle.
Extrabinomial variation
Neurobiol., 59:107–128.
greater variability in repeat estimates of a population proportion than would be expected if the population had a binomial distribution.
Crofton, K.M.
Frameshift mutation
Crofton, K.M., Sheets, L.P.
a genetic mutation caused by insertions or deletions of a number of nucleotides that is not evenly divisible by three within a DNA sequence that codes for a protein/peptide.
Toxicol., 8:199–211.
Insertion
Crofton, K.M, Lassiter, T.L, Rebert, C.S.
the addition of one or more nucleotide base pairs into a DNA sequence.
Res.,80:25–30.
Jackpot
Ison, J.R.
a large number of mutants that arose through clonal expansion from a single mutation.
Mattsson, J.L., Boyes, W.K., Ross, J.F.
Large deletions
Peele, D.B., Allison, S.D., Crofton, K.M.
deletions in DNA of more than several kilobases (which are effectively detected with the Spi- selection and the lacZ plasmid assays).
Pharmacol., 105:321–332.
Ligation
Bammer, G. (1982) Pharmacological investigations of neurotransmitter involvement in passive avoidance responding:
the covalent linking of two ends of DNA molecules using DNA ligase.
Rev., 6:247–296.
Mitogen
Bushnell, P.J.
a chemical that stimulates a cell to commence cell division, triggering mitosis (i.e. cell division).
Teratol., 10:237–244.
Packaging
Kucharski, D., Spear, N.E.
the synthesis of infective phage particles from a preparation of phage capsid and tail proteins and a concatamer of phage DNA molecules.
Psychobiol., 17:465–479.
Commonly used to package DNA cloned onto a lambda vector (separated by cos sites) into infectious lambda particles.
Morris, R. (1984) Developments of a water-maze procedure for studying spatial learning in the rat.
Packaging efficiency
Methods, 11:47–60.
the efficiency with which packaged bacteriophages are recovered in host bacteria.
Brandeis, R., Brandys, Y., Yehuda, S. (1989) The use of the Morris water maze in the study of memory and learning.
Plaque forming unit (pfu)
Int.
a measure of viable bacteriophage numbers.
J. Neurosci., 48:29–69.
Positive selection
Teratol., 9:235–241.
a method that permits only mutants to survive.
Toxicol., 20:387–399.
Reporter gene
Akaike, M., Tanaka, K., Goto, M., Sakaguchi, T. (1988) Impaired Biel and Radial arm maze learning in rats with methyl-nitrosurea induced microcephaly.
a gene whose mutant gene product is easily detected.
Teratol., 10:327–332.
Sampling time
Cory-Slechta, D.A., Weiss, B., Cox, C. (1983) Delayed behavioral toxicity of lead with increasing exposure concentration.
the end of the period of time, prior to sacrifice, during which the chemical is not administered and during which unprocessed DNA lesions are fixed into stable mutations.
Pharmacol., 71:342–352.
accordingly, DNA inserted into a shuttle vector can be tested or manipulated in two different cell types or two different organisms.
Prophet, E.B., Mills, B., Arrington, J.B., Sobin, L.H.
Transgenic
Laboratory Methods in Histotechnology, American Registry of Pathology, Washington, DC, s. 84–107.
of, relating to, or being an organism whose genome has been altered by the transfer of a gene or genes from another species.’
Bancroft, J.D., Gamble, M. (2002) Theory and Practice of Histological Techniques, 5th edition, Churchill Livingstone, London.
Depending on the sensitivity of cognitive function tests, investigation of a large higher number of animals should be considered e.g. up to 1 male and 1 female per litter (for animal assignments see Appendix 1) (further guidance on sample size is provided in the OECD Guidance Document 43 (8)).
Fix, A.S., Ross, J.F., Stitzel, S.R., Switzer, R.C.
This table presents the minimum number of times when measurements should be performed.
Schmued, L.C., Hopkins, K.J.
Depending on the anticipated effects, and the results of the initial measurements, it may be advisable to add additional time points (e.g. aged animals) or to perform the measurements in other developmental stages.
Brain Res., 874:123–130.
It is recommended that pups not be tested during the two days after weaning (see paragraph 32).
Krinke, G.J., Classen, W., Vidotto, N., Suter, E., Wurmlin, C.H.
Recommended ages for adolescent testing are:
Pathol., 53:365–372.
learning and memory = PND 25 ± 2;
De Olmos, I.S., Beltramino, C.A. och de Olmos de Lorenzo, S. (1994) Use of an amino-cupric-silver technique for the detection of early and semiacute neuronal degeneration caused by neurotoxicants, hypoxia and physical trauma.
motor and sensory function = PND 25 ± 2.
Teratol., 16, 545–561.
Recommended ages for testing young adults is PND 60-70.
De Groot, D.M.G., Bos-Kuijpers, M.H.M., Kaufmann, W.S.H., Lammers, J.H.C.M., O'Callaghan, J.P., Pakkenberg, B., Pelgrim, M.T.M., Waalkens-Berendsen, I.D.H., Waanders, M.M., Gundersen, H.J.
Body weights should be measured at least twice weekly when directly dosing pups for adjustment of doses at a time of rapid body weight gain.
Pharmacol., 19:745–755.
Brain weights and neuropathology may be assessed at some earlier time (e.g. PND 11), if appropriate (see paragraph 39).
De Groot, D.M.G., Hartgring, S., van de Horst, L., Moerkens, M., Otto, M., Bos-Kuijpers, M.H.M., Kaufmann, W.S.H., Lammers, J.H.C.M., O'Callaghan, J.P., Waalkens-Berendsen, I.D.H., Pakkenberg, B., Gundersen, H.J.
Other developmental landmarks in addition to the body weight (e.g. eye opening) should be recorded when appropriate (see paragraph 31).
Toxicol., 20:417–432.
See paragraph 35.
Rodier, P.M., Gramann, W.J.
The threshold CV for a given tissue was identified from a graph of CV values — arranged from smallest sequentially to largest — for all means from all experiments in the validation exercise using a specific model (agonist or antagonist).
Howard, C.V., Reed, M.G.
The threshold CV was read from the point at which the increments between to the next highest CVs in the series are dramatically larger than the preceding few CVs- the “breakpoint”.
Hyman, B.T., Gomez-Isla, T., Irizarry, M.C.
It should be noted that although this analysis identified relatively reliable “breakpoints” for the antagonist model of the assay, CV curves for the agonist assay showed a more uniform increase making identification of a threshold CV by this method somewhat arbitrary.
Korbo, L., Andersen, B.B., Ladefoged, O., Møller, A. (1993) Total numbers of various cell types in rat cerebellar cortex estimated using an unbiased stereological method.
Research has shown the mammary gland, especially in early life mammary gland development, to be a sensitive endpoint for oestrogen action.
Schmitz, C. (1997) Towards more readily comprehensible procedures in disector stereology.
It is recommended that endpoints involving pup mammary glands of both sexes be included in this test method, when validated.
J. Neurocytol., 26:707–710.
“New batch” refers to a fresh batch of cells received from ATCC.
West, M.J.
“Frozen batch” refers to cells that have been previously cultured and then frozen at a laboratory other than ATCC.
Trends Neurosci., 22:51–61.
If extraction is required, three replicate measurements are made for each extract.
Schmitz, C., Hof, P.R.
Each sample will be extracted only once.
Gavin, C.E., Kates, B., Gerken, L.A., Rodier, P.M. (1994) Patterns of growth deficiency in rats exposed in utero to undernutrition, ethanol, or the neuroteratogen methylazoxymethanol (MAM).
If greater basal hormone production can be achieved the limit can be greater.
Ohno, M., Aotani, H., Shimada, M. (1995) Glial responses to hypoxic/ischemic encephalopathy in neonatal rat cerebrum.
Some T and E2 antibodies may cross-react with androstendione and oestrone, respectively, at a greater percentage.
Brain Res., 84:294–298.
In such cases it is not possible to accurately determine effects on 17β-HSD.
Jensen KF, Catalano SM.
However, the data can still provide useful information regarding the effects on oestrogen or androgen production in general.
Ikonomidou, C., Bosch, F., Miksa, M., Bittigau, P., Vöckler, J., Dikranian, K., Tenkova, T.I., Stefovska, V., Turski, L., Olney, J.W.
In such cases data should be expressed as androgen/oestrogen responses rather than E2 and T.
Science, 283:70–74.
These include:
Ikonomidou, C., Bittigau, P., Ishimaru, M.J., Wozniak, D.F., Koch, C., Genz, K., Price, M.T., Sefovska, V., Hörster, F., Tenkova, T., Dikranian, K., Olney, J.W.
cholesterol, pregnenolone, progesterone, 11-deoxycorticosterone, corticosterone, aldosterone, 17α-pregnenolone,17α-progesterone, deoxycortisol, cortisol, DHEA, androstenedione, oestrone.
Friede, R. L. (1989) Developmental Neuropathology.
Solvent (DMSO) control (0), 1 μl DMSO/well.
House, D.E., Berman, E., Seeley, J.C., Simmons, J.E.
+, positive
Let., 63:127–133.
Cells in Blank wells receive medium only (i.e. no solvent).
Tilson, H.A., MacPhail, R.C., Crofton, K.M.
Methanol (MeOH) will be added after the exposure is terminated and the medium is removed from these wells.
Health Perspect., 104:401–405.
DMSO solvent control (1 μl/well).
US EPA (2005) Guidelines for Carcinogen Risk Assessment.
Confirm previous run using the same experimental design.
US EPA (1996) Guidelines for Reproductive Toxicity Risk Assessment, Federal Register 61(212):
Re-run assay at 1/2-log concentration spacing (bracketing the concentration that tested significantly different in the preceding experiment).
56274–56322.
Fold-change at one concentration is statistically significantly different from the SC
Danish Environmental Protection Agency (1995) Neurotoxicology.
Refers to replicate measures of the same sample
Muller, K.E., Barton, C.N., Benignus, V.A.
José Manuel Barroso
Neurotoxicology, 5:113–126.
A developmental neurotoxicity study can be conducted as a separate study, incorporated into a reproductive toxicity and/or adult neurotoxicity study (e.g. test methods B.34 (14), B.35 (15), B.43 (16)), or added onto a prenatal developmental toxicity study (e.g. test method B.31 (17)).
Gad, S.C.
When the developmental neurotoxicity study is incorporated within or attached to another study, it is imperative to preserve the integrity of both study types.
Toxicol., 08:21–27.
All testing should comply with applicable legislation or government and institutional guidelines for the use of laboratory animals in research (e.g. 18).
Abby, H., Howard, E. (1973) Statistical procedures in developmental studies on a species with multiple offspring.
The testing laboratory should consider all available information on the test chemical prior to conducting the study.
Psychobiol., 6:329–335.
Such information will include the identity and structure of the chemical; its physico-chemical properties;
Haseman, J.K., Hogan, M.D.
the results of any other in vitro or in vivo toxicity tests on the chemical; toxicological data on structurally related chemicals;
Teratology, 12:165–172.
and the anticipated use(s) of the chemical.
Holson, R.R., Pearce, B. (1992) Principles and pitfalls in the analysis of prenatal treatment effects in multiparous species.
This information is necessary to satisfy all concerned that the test is relevant for the protection of human health, and will help in the selection of an appropriate starting dose.
Nelson, C.J., Felton, R.P., Kimmel, C.A., Buelke-Sam, J., Adams, J. (1985) Collaborative Behavioral Teratology Study:
The route of administration will generally be oral (e.g.gavage, dietary, via drinking water), but other routes (e.g. dermal, inhalation) may be used depending on the characteristics and anticipated or known human exposure routes (further guidance is provided in the Guidance Document 43(8)).
Crofton, K.M., Makris, S.L., Sette, W.F., Mendez, E., Raffaele, K.C.
Justification should be provided for the route of administration chosen.
Teratol., 26:345–352.
The test chemical should be administered at approximately the same time every day.
Bolon, B., Garman, R., Jensen, K., Krinke, G., Stuart, B., and an ad hoc working group of the STP Scientific and Regulatory Policy Committee.
For offspring killed through PND 22, brain tissues should be evaluated; for animals killed at termination, both central nervous system (CNS) tissues and peripheral nervous system (PNS) tissues should be evaluated.
Tamura, R.N., Buelke-Sam, J. (1992) The use of repeated measures analysis in developmental toxicology studies.
OECD (1995).
Teratol., 14(3):205–210.
Copenhagen, Denmark, 13-14 June 1995.
Tukey, J.W., Ciminera, J.L., Heyse, J.F.
US EPA (1998).
Biometrics, 41:295–301.
Available:
Crofton, K.M., Foss, J.A., Haas, U., Jensen, K., Levin, E.D., and Parker, S.P.
Cory-Slechta, D.A., Crofton, K.M., Foran, J.A., Ross, J.F., Sheets, L.P., Weiss, B., Mileson, B. (2001).
Neurotoxicology and Teratology, 30(4):266–287.
Health Perspect., 109:79-91.
Neurotoxicology and Teratology, 30(4):288–325.
Dorman, D.C., Allen, S.L., Byczkowski, J.Z., Claudio, L., Fisher, J.E.
Holson, R.R., Freshwater, L., Maurissen, J.P.J., Moser, V.C., and Phang, W.
Health Perspect., 109:101-111.
Neurotoxicology and Teratology, 30(4):326–348.
Garman, R.H., Fix,A.S., Jortner, B.S., Jensen, K.F., Hardisty, J.F., Claudio, L., Ferenc, S. (2001).
Tyl, R.W., Crofton, K.M., Moretto, A., Moser, V.C., Sheets, L.P., and Sobotka, T.J.
Health Perspect., 109:93-100.
Neurotoxicology and Teratology, 30(4):349–381.
OECD (2003).
Livmoderviktsresponsen kommer att jämföras med etablerade historiska data (se hänvisning 5).
Washington D.C., US, 23-25 October 2000.
Om denna positiva grundkontrollstudie inte ger förväntade resultat bör försöksbetingelserna granskas och ändras.
July 2008 Available:
Owens JW, Ashby J. (2002).
Kimmel, C.A., Rees, D.C., Francis, E.Z.
32:445–520.
Teratol., 12: 173-292.
OECD (2006).
Experimental and Clinical Neurotoxicology, 2nd Edition, ISBN 0195084772, Oxford University Press, New York.
Kanno, J, Onyon L, Haseman J, Fenner-Crisp P, Ashby J, Owens W.
Mendola, P., Selevan, S.G., Gutter, S., Rice, D. (2002) Environmental factors associated with a spectrum of neurodevelopmental deficits.
109:785–94.
Slikker, W.B., Chang, L.W.
Phase 2 – Testing of Potent and Weak Oestrogen Agonists by Multiple Laboratories.
Handbook of Developmental Neurotoxicology, 1st Edition, ISBN 0126488606, Academic Press, New York.
Kanno J, Onyon L, Peddada S, Ashby J, Jacob E, Owens W.
WHO (1986) Principles and Methods for the Assessment of Neurotoxicity Associated with Exposure to Chemicals, (Environmental Health Criteria 60), Albany, New York:
Phase Two – Dose Response Studies.
Approaches and Methods, 1st Edition, ISBN 012168055X, Academic Press, New York.
Health Persp.111:1550–1558.
De Cabo, C., Viveros, M.P.
Owens W, Ashby J, Odum J, Onyon L. (2003).
Teratol., 19:499-509.
Phase Two – Dietary phytoestrogen analyses.
Agnish, N.D., Keller, K.A.
111:1559–1567.
Toxicol., 38:2-6.
Ogasawara Y, Okamoto S, Kitamura Y, Matsumoto K. (1983).
Avery, D.L., Spyker, J.M.
Endocrinology 113:582–587.
Animal Sci., 27:110-112.
Branham WS, Sheehan DM, Zehr DR, Ridlon E, Nelson CJ.
Wier, P.J., Guerriero, F.J., Walker, R.F.
Endocrinology 117:2229–2237.
Implementation of a primary screen for developmental neurotoxicity.
Schlumpf M, Berger L, Cotton B, Conscience-Egli M, Durrer S, Fleischmann I, Haller V, Maerkel K, Lichtensteiger W.
Toxicol., 13:118-136.
127:10–15.
Spear, N.E., Campbell, B.A.
Zarrow MX, Lazo-Wasem EA, Shoger RL.
Krasnegor, N.A., Blass, E.M., Hofer, M.A., Smotherman, W.
Science 118:650–651.
A Psychobiological Perspective.
Drane HM, Patterson DSP, Roberts BA, Saba N. (1975).
Zoetis, T., Walls, I. (2003) Principles and Practices for Direct Dosing of Pre-Weaning Mammals in Toxicity Testing and Research.
13:425–427.
Moser, V., Walls, I., Zoetis, T. (2005) Direct dosing of preweaning rodents in toxicity testing and research:
Boettger-Tong H, Murphy L, Chiappetta C, Kirkland JL, Goodwin B, Adlercreutz H, Stancel GM, Makela S. (1998).
Int.
Health Perspec.106:369–373.
J. Toxicol., 24:87-94.
OECD (2007).
Conolly, R.B., Beck, B.D., Goodman, J.I.
128:145–157.
Detection of Toxicity to Reproduction for Medical Products (S5A).
41:1517–1525.
International Conference on Harmonisation of Technical Requirements for Registration of Phamaceuticals for Human Use.
Yamasaki K, Sawaki M, Noda S, Wada T, Hara T, Takatsuki M. (2002).
Lochry, E.A.
76:613–620.
Toxicol., 6:433-439.
Thigpen JE, Haseman JK, Saunders HE, Setchell KDR, Grant MF, Forsythe D. (2003).
Tachibana, T., Narita, H., Ogawa, T., Tanimura, T. (1998) Using postnatal age to determine test dates leads to misinterpretation when treatments alter gestation length, results from a collaborative behavioral teratology study in Japan.
53:477–485.
Teratol., 20:449-457.
Ashby J, Tinwell H, Odum J, Kimber I, Brooks AN, Pate I, Boyle CC.
Gallavan, R.H.
Toxicol.20:343–347.
Toxicol., 13:383-390.
Thigpen JE, Lockear J, Haseman J, Saunders HE, Caviness G, Grant MF, Forsythe DB.
Gray, L.E.
26:381–393.
Sci., 58:350-365.
Thigpen JE, Li L-A, Richter CB, Lebetkin EH, Jameson CW.
Teratol., 7:579-586.
Acute oral toxicity – up-and-down procedure.
Korenbrot, C.C., Huhtaniemi, I.T., Weiner, R.W.
OECD (2000).
Spear, L.P.
Bulbring, E., and Burn, J.H.
Teratol., 12:489-95.
Dorfman, R.I., Gallagher, T.F. och Koch, F.C (1936).
Behav., 23:896-920.
Jones, R.C. och Edgren, R.A.
Adams, J. (1986) Methods in Behavioral Teratology.
OECD (1982).
Reiter, L.W., MacPhail, R.C.
Organization for Economic Co-operation and Development – Principles of Good Laboratory Practice, ISBN 92-64-12367–9, Paris.
A survey of methods with potential use in toxicity testing.
Dorfman R.I.
Toxicol., 1:53-66.
Thigpen J. E. et al.
Robbins, T.W.
Gray L.E. och Ostby J. (1998).
A critique of the methods available for the measurement of spontaneous motor activity, Handbook of Psychopharmacology, Vol.
Booth AN, Bickoff EM och Kohler GO.
7, Iverson, L.L., Iverson, D.S., Snyder, S.H., (eds.)
Science 131:1807–1808.
Plenum Press, New York, pp. 37-82.
Kato H, Iwata T, Katsu Y, Watanabe H, Ohta Y, Iguchi T (2004).
Crofton, K.M., Peele, D.B., Stanton, M.E.
52, 1410–1414.
Ruppert, P.H., Dean, K.F., Reiter, L.W.
Dorfman RI (1962).
Psychobiol., 18:247-260.
Gray LE Jr, Furr J och Ostby JS (2005).
Crofton, K.M., Howard, J.L., Moser, V.C., Gill, M.W., Reiter, L.W., Tilson, H.A., MacPhail, R.C.
Current Protocols in Toxicology 16.9.1–16.9.15.
Teratol., 13:599-609.
Owens, W, Zeiger E, Walker M, Ashby J, Onyon L, Gray, Jr, LE (2006).
Teratol., 19:1997.
Owens W, Gray LE, Zeiger E, Walker M, Yamasaki K, Ashby J, Jacob E (2007).
405-411.
115(5):671–8.
Handley, D.E., Ross, J.F., Carr, G.J.
Korenchevsky V (1932).
A force plate system for measuring low-magnitude reaction forces in small laboratory animals.Physiol.
Biochem J26:413–422.
Behav., 64:661-669.
Korenchevsky V, Dennison M, Schalit R (1932).
Edwards, P.M., Parker, V.H.
Biochem J26:1306–1314.
A simple, sensitive, and objective method for early assessment of acrylamide neuropathy in rats.
Eisenberg E, Gordan GS (1950).
Pharmacol., 40:589-591.
J Pharmacol Exp Therap 99:38–44.
Davis, M. (1984) The mammalian startle response.
Eisenberg E, Gordan GS, Elliott HW (1949).
Koch, M. (1999) The neurobiology of startle.
Endocrinology 45:113–119.
Neurobiol., 59:107-128.
Hershberger L, Shipley E, Meyer R (1953).
Crofton, K.M.
Proc Soc Exp Biol Med 83:175–180.
Crofton, K.M., Sheets, L.P.
Hilgar AG, Vollmer EP (1964).
Crofton, K.M, Lassiter, T.L, Rebert, C.S.
Academic Press, 151–220.
Res.,80:25-30.
Massaro EJ (2002).
Ison, J.R.
Humana Press, s 38.
Teratol., 6:437–445.
Supplemental materials for Owens et al.
Mattsson, J.L., Boyes, W.K., Ross, J.F.
Korea Food and Drug Administration.
Peele, D.B., Allison, S.D., Crofton, K.M.
OECD (2009).
Pharmacol., 105:321-332.
För reproduktiva endpoints är det tänkt att, som ett första steg och när det är tillgängligt, information från studier med upprepad dosering (inklusive screening av reproduktionstoxicitetsstudier, t.ex.OECD:s TG 422 [se hänvisning 32]), eller kortvariga screeningtester av endokrinstörande ämnen (t.ex.uterotrof assay – testmetod B.54 [se hänvisning 36] och Hershbergers bioassay – testmetod B.55 [se hänvisning 37]) används för att påvisa effekter på fortplantningsorganen hos hanar och honor.
A review and some new results.
Den utökade engenerationsstudien av reproduktionstoxicitet fungerar sedan som ett test för reproduktionsendpoints som kräver interaktion mellan hanar och honor, honor och befruktade ägg, honor och avkomma samt F1-generationen tills efter könsmognaden (se OECD:s vägledning 151 som stöder denna testmetod [hänvisning 40]).
Teratol., 10:237-244.
Behandlingen före parning bör pågå tillräckligt länge för att uppnå ett stabilt tillstånd vad gäller exponeringsförhållandena hos P-hanar och -honor.
Green, R.J., Stanton, M.E.
Hanar och honor i samma dosgrupp bör saminhysas (undvik att para ihop syskon) i upp till två veckor, med början på PND 90 eller senare, men senast PND 120.
Neurosci., 103:98-105.
Förfarandena bör vara desamma som för P-djuren.
Kucharski, D., Spear, N.E.
Systemiska effekter bör övervakas hos P-djur.
Morris, R. (1984) Developments of a water-maze procedure for studying spatial learning in the rat.
De ska förvaras under lämpliga förhållanden och utsättas för partiell eller fullskalig hematologi, klinisk biokemi, test av T4 och TSH eller andra undersökningar som föranleds av testkemikaliens kända biverkningsprofil (se OECD:s vägledning 151 [hänvisning 40]).
Brandeis, R., Brandys, Y., Yehuda, S. (1989) The use of the Morris water maze in the study of memory and learning.
Organ som visar behandlingsrelaterade förändringar bör också undersökas hos alla djur i de lägre dosgrupperna för att hjälpa till att fastställa ett Noael-värde.
Int.
Cooper, R.L., J.C. Lamb, S.M.
J. Neurosci., 48:29-69.
Thigpen, J.E., K.D.R.
D'Hooge, R., De Deyn, P.P.
Zoetis, T. and I. Walls (2003), Principles and Practices for Direct Dosing of Pre-Weaning Mammals in Toxicity Testing and Research, ILSI Press, Washington, DC.
Vorhees, C.V.
Conolly, R.B., B.D.
A comparison of performance in two water mazes in progeny prenatally exposed to different doses of phenytoin.
Ulbrich, B. och A.K.
Toxicol., 20:387-399.
Creasy, D.M.
Akaike, M., Tanaka, K., Goto, M., Sakaguchi, T. (1988) Impaired Biel and Radial arm maze learning in rats with methyl-nitrosurea induced microcephaly.
Goldman, J.M., A.S.
Cory-Slechta, D.A., Weiss, B., Cox, C. (1983) Delayed behavioral toxicity of lead with increasing exposure concentration.
Korenbrot, C.C., I.T.
Pharmacol., 71:342-352.
Ladics, G.S.
J. Gerontol., 36:338–341.
Robb, G.W., R.P.
Fix, A.S, Garman, R.H.
Klinefelter, G.R., L.E.
Prophet, E.B., Mills, B., Arrington, J.B., Sobin, L.H.
Klinefelter, G.R., N.L.
Bancroft, J.D., Gamble, M. (2002) Theory and Practice of Histological Techniques, 5th edition, Churchill Livingstone, London.
Slott, V.L. och S.D.
Fix, A.S., Ross, J.F., Stitzel, S.R., Switzer, R.C.
Toth, G.P., J.A.
Pathol., 24: 291-304.
Linder, R.E., L.F.
Schmued, L.C., Hopkins, K.J.
Thigpen, JE, K.D.R.
A high affinity tracer for the localization of neuronal degeneration.
Tyl, R.W., K. Crofton, A. Moretto, V. Moser, L.P.
Krinke, G.J., Classen, W., Vidotto, N., Suter, E., Wurmlin, C.H.
OECD (2013), Guidance Document supporting TG 443: Extended One Generation Reproductive Toxicity Study, Series on Testing and Assessment, No.
Pathol., 53:365-372.
Specifikt ska de kemikalier som testas inkludera den starka induceraren forskolin (CAS-nr 66575-29-9), den starka hämmaren prokloraz (CAS-nr 67747-09-5), den måttliga induceraren atrazin (CAS-nr 1912-24-9), den måttliga hämmaren aminoglutetimid (CAS-nr 125-84-8), den svaga induceraren (E2-produktion) och den svaga hämmaren (T-produktion) bisfenol A (CAS-nr 80-05-7) samt den negativa kemikalien mänskligt korioniskt gonadotropin (HCG) (CAS-nr 9002-61-3), såsom visas i tabell 2.
De Olmos, I.S., Beltramino, C.A., and de Olmos de Lorenzo, S. (1994) Use of an amino-cupric-silver technique for the detection of early and semiacute neuronal degeneration caused by neurotoxicants, hypoxia and physical trauma.
HKG