EPA-600/1-78-014
February  1978
Environmental Health Effects Research Series
           SCREENING METHODS FOR TOXIC SUBSTANCES

                                                Health Effects Research Laboratory
                                               Office of Research and Development
                                              U.S. Environmental Protection Agency
                                        Research Triangle Park, North Carolina 27711

-------
                RESEARCH REPORTING SERIES

Research reports of the Office of Research and Development, U.S. Environmental
Protection Agency, have been grouped into nine series. These nine broad cate-
gories were established to facilitate further development and application of en-
vironmental technology.  Elimination of traditional grouping  was consciously
planned to foster technology transfer and a maximum interface in related fields.
The nine series are:

      1.  Environmental  Health Effects Research
      2.  Environmental  Protection Technology
      3.  Ecological Research
      4.  Environmental  Monitoring
      5.  Socioeconomic Environmental Studies
      6.  Scientific and Technical Assessment Reports (STAR)
      7.  Interagency Energy-Environment Research and Development
      8.  "Special" Reports
      9.  Miscellaneous Reports
This report has been assigned to the ENVIRONMENTAL HEALTH EFFECTS RE-
SEARCH series. This series describes projects and studies relating to the toler-
ances of man  for unhealthful substances or conditions. This work is generally
assessed from a medical viewpoint, including physiological or psychological
studies. In addition to toxicology and other medical specialities, study areas in-
clude biomedical  instrumentation and health research techniques utilizing ani-
mals — but always with  intended application to human health measures.
  This document is available to the public through the National Technical Informa-
  tion Service, Springfield, Virginia 22161.

-------
                                EPA-600/1-78-014
                                February 1978
SCREENING METHODS FOR TOXIC SUBSTANCES
                  by

            Harish C. Sikka
     Syracuse Research Corporation
       Syracuse, New York 13210
        Contract No. 68021786
            Project Officer

             Larry L. Hall
   Environmental Toxicology Division
  Health Effects Research Laboratory
  Research Triangle Park, N.C. 27711
 U.S. ENVIRONMENTAL PROTECTION AGENCY
  OFFICE OF RESEARCH AND DEVELOPMENT
  HEALTH EFFECTS RESEARCH LABORATORY
  RESEARCH TRIANGLE PARK, N.C. 27711

-------
                            DISCLAIMER
     This report has been reviewed by the Health Effects Research
Laboratory, U.S. Environmental Protection Agency, and approved
for publication.  Approval does not signify that the contents
necessarily reflect the views and policies of the U.S. Environmental
Protection Agency, nor does mention of trade names or commercial
products consitute endorsement or recommendation for use.
                                 ii

-------
                                  FOREWORD
     The many benefits of our modern, developing, industrial society are
accompanied by certain hazards.  Careful assessment of the relative risk of
existing and new man-made environmental hazards is necessary for the estab-
lishment of sound regulatory policy.  These regulations serve to enhance
the quality of our environment in order to promote the public health and
welfare and the productive capacity of our Nation's population.

     The Health Effects Research Laboratory, Research Triangle Park,
conducts a coordinated environmental health research program in toxicology,
epidemiology, and clinical studies using human volunteer subjects.  These
studies address problems in air pollution, non-ionizing radiation, environ-
mental carcinogenesis and the toxicology of pesticides as well as other
chemical pollutants.  The Laboratory develops and revises air quality
criteria documents on pollutants for which national ambient air quality
standards exist or are proposed, provides the data for registration of new
pesticides or proposed suspension of those already in use, conducts research
on hazardous and toxic materials, and is preparing the health basis for
non-ionizing radiation standards.  Direct support to the regulatory function
of the Agency is provided in the form of expert testimony and preparation
of affidavits as well as expert advice to the Administrator to assure the
adequacy of health care and surveillance of persons having suffered imminent
and substantial endangerment of their health.

     The objective of this project was to explore the feasibility of using
fluorescent probes as a technique for detecting effects produced by the
action of neurotoxic chemicals.  This approach may ultimately provide a
more sensitive test for adverse biological effects needed in the hazard
evaluation of agricultural and other chemicals.
                                      John H. Knelson, M.D.
                                            Director,
                               Health Effects Research Laboratory
                                     iii

-------
                                  ABSTRACT






     The present report deals with the application of fluorescent probe




technique to the detection of conformational changes in rat brain synaptosomes




under the influence of certain neurotoxic chemicals, chlorophenothane (DDT)




and diphenylhydantoin, which are expected to produce functional changes in




nerve membranes.  Pretreatment of the rats with (1) a single dose of DDT




capable of producing neurological symptoms and (ii) repeated sub-lethal




doses of DDT did not alter the fluorescence characteristics of the hydro-




phobic probe 8-anilino-l-naphthalene sulfonic acid (ANS) bound to the




synaptosomes.  DDT treatment also showed no effect on native protein




fluorescence of synaptosomes.




     Exposure of synaptosomes to diphenylhydantoin in vitro did not induce




conformational changes as measured by ANS and intrinsic fluorescence.
                                     iv

-------
                                  CONTENTS




Disclaimer	     ii




Foreword	    iii




Abstract   	     iv




     I                    '                                                ';




     1.   INTRODUCTION   . . .	       1




          General  	       1




          Objectives 	       2




     2.   CONCLUSIONS   	       3




     3.   MATERIALS AND METHODS   	       A




     4.   EXPERIMENTAL PROCEDURES   	  	       7




     5.   RESULTS	       9




References    	     16

-------
                                 SECTION 1




                                INTRODUCTION






GENERAL




     A large number of industrial and agricultural chemicals including




pesticides, detergents, solvents, plastics, chemical Intermediates, and




plasticizers may be introduced into the environment as effluents from




manufacturing plants, or during their use and disposal.  Among the major




concerns associated with the presence of these chemicals in the environment




is their potential toxicity to man.  From a toxicological standpoint, the




nervous system is one of the more sensitive sites of action of various




environmental contaminants.




     At present, a toxicological evaluation of neurotoxic chemicals usually




consists of measuring a given organism's behavioral response, neurophysio-




logical activity and examining pathological changes in the nervous system.




These methods are suitable for detecting neurotoxic disorders resulting




from acute or chronic toxicity, but may not be able to detect subtle effects




or a minimal degree of damage resulting from low-level exposure to these




chemicals.  Evidence has been presented which shows that subclinical nerve




damage was detected in workers exposed to lead who showed no clinical




neurological symptoms. »   Therefore, reliable, sensitive techniques are




needed to detect early damage resulting from a variety of neurotoxic




substances.

-------
     Although various neurotoxic substances like DDT, nicotine,  pyrethroids,




tetrodotoxin and methylmercury act via different mechanisms, an effect upon




the nerve membrane as a whole is implicated with all of them.3'4        It




is generally believed that these chemicals interact specifically or non-




specifically with components of the nerve membrane, thereby leading to




possible changes in membrane function.  Such changes may account for the




neurophysiological effects  of these chemicals.  It is conceivable that such




alterations may be preceded by changes in the conformation or structural




organization of the nerve membrane.  The conformational changes could there-




fore be used as an indicator of neurotoxicity.




     In recent years, fluorescent probes have been employed for detecting




structural or conformational changes in membranes and other biological




structures.8'9'10'11'12'13  The high sensitivity of fluorescent  probes to their




microenvironment permits one to detect relatively low levels of alteration




which cannot be discerned by biochemical or physiopathological methods.




The objective of this investigation was to explore the feasibility of using




fluorescent probes as a sensitive technique for detecting effects produced




by the action of neurotoxic chemicals.




OBJECTIVES




1.   To examine if selected neurotoxic chemicals induce conformational




     changes in nerve cells or their components in vivo, using fluorescent




     probes.




2.   To establish the usefulness of fluorescent probes as a tool for




     predicting neurotoxicological hazards.

-------
                                 SECTION 2




                                CONCLUSIONS






     The present investigation was undertaken to determine whether DDT,




a neurotoxic pesticide, produces conformational changes in nerve membranes




and if these changes can be detected by fluorescent probes.  It has been




shown that DDT alters ion permeability in nerve membranes.5  Hilton et al.3




and Hilton and O'Brien14 have postulated that the mechanism by which DDT




alters nerve membrane permeability involves modification of the membrane




structure.  It may be postulated that DDT, on account of its high lipid




solubility, may expand cellular membranes leading to an alteration in their




structure as has been reported for certain nonspecific lipid-soluble drugs.6




     In the present study, using brain synaptosomes as a model system, we




have demonstrated that any structural or conformational changes produced




by DDT can not be detected by fluorescent probe technique  suggesting that




the technique is not a sensitive indicator of DDT-induced  toxicity.  This




evaluation of the fluorescent probes is based on the assumption that the




pesticide at the concentrations tested did induce changes  in the  structure




of the synaptosomes.

-------
                                 SECTION 3


                           MATERIALS AND METHODS



Preparation of Brain Subcellular Fractions


     Brain synaptosomes were prepared from male Sprague-Dawley rats fed


ad_ libitum and weighing 200-250g.  The animals were sacrificed by decapita-


tion, the brain was excised and placed in cold (4°C) homogenizing medium.

                                   '                       -
Rat brain synaptosomes were prepared according to the method of Gray and


Whittaker. **  The brain tissue was disrupted by homogenization in 0.32 M


sucrose.  The crude mitochondrial fraction was separated  from the cell


debris, red blood cells, nuclei and soluble fraction by means of differ-


ential centrifugation.  Synaptosomes, free mitochondria,  and myelin were


then separated by means of density-gradient centrifugation.  The scheme


for the isolation of various subcellular fractions is outlined in


Figures 1 and 2.


     The protein content of synaptosomes was determined according to the


method of Lowry et^ al.



Fluorescence .Measurements


     Fluorescence measurements were made with an Aminco-Keirs spectro-


photofluorometer (American Instruments Company) using an  X-Y recorder.  The


light source was a Xenon lamp.  Measurements were made at 25°C in a temper-


ature-controlled cell holder connected to a circulating water bath.


Aliquots of synaptosomal preparations were resuspended in 0.32 M sucrose

-------
in 15 mM Trls-HCl buffer (pH 7.4) before making fluorescence measurements.
The final synaptosome concentration was approximately 75 wg/ml unless
indicated otherwise.  An aliquot of ANS (8-anilino-l-naphthalene sulfonic
acid) stock solution was then added to give a final probe concentration of
3.2 X 10  M, unless indicated otherwise.  The fluorescence measurements
were carried out at wavelengths corresponding to excitation and emission
maxima determined by analysis of the spectrum of ANS bound to the
synaptosomes.
     ANS was obtained from Eastman Kodak and was recrystallized twice from
boiling water before use.
Brain homogenate
                    -Pi (nuclei and cell debris)
                  -P2
~A (ravelin fragments)
 -B (nerve-ending particles)
_C (mitochondria)
                   —P3  (microsomes)
                   —Pi+  (ribosomes: post-microsomal fraction)
     Figure 1.  Nomenclature used in describing subcellular  fractions.

-------
           Homogenate of brain tissue 10% (w/v) in 0.32 M sucrose

                     centrifuged at lOOOg for 10 minutes
                I
          Precipitate
                V
  Washed twice by resuspension
     in 0.32 M sucrose and
    re-centrifuging as above
                f
    Separated in a density
        gradient to give
        three fractions
Layer between
0.32 and 0.8 M
sucrose
centrifuged
at 105g for
60 min.
Layer between
0.8 and 1.2 M
sucrose
diluted with
equal vols.
of water,
centrifuged
at 105g for
60 min.
                                Washings added
                                to supernatant
                                                         ->
                                                Supernatant centrifuged
                                                  at 17000g for 55 min.
                                                           \/
                                                Supernatant centrifuged
                                                   at 105g for 60 min.


Pellet
below
1.2 M
sucrose
                                                            Supernatant
                                                         centrifuged at 10bg
                                                            for 120 min.
                                                 1

                                                *
                                                          Final supernatant
                                                             (discarded)
                      B
Figure 2.  Scheme summarizing preparation of subcellular fractions.

                                       6

-------
                                 SECTION 4




                          EXPERIMENTAL PROCEDURES






Method of Tissue or Cell Treatment




     Since absorption, distribution, excretion, and metabolism of a chemical




determine its toxicity to the animal, it is desirable to expose the animal




to the test chemical in vivo followed by in vitro testing to determine if




the chemical produces any effect.  The rats were exposed to the toxic




substance, following which suitable tissues were removed and examined for




possible conformational changes.






Selection of Cell and/or Cell Components Examined for Possible Conformational




Changes




     The techniques for measuring conformational changes using fluorescent




probes, reproducibly and without complicated instrumentation requires that




the biological material be in suspension.  This precludes the use of brain




slices or axons.  In the present studies, which were designed to examine




an overall effect of a given chemical on cell structure, it was desirable




to use an isolated intact cell  system in order to detect the possible




conformational changes occurring in the whole nerve cell as well as its




components.  However, since techniques for the preparation of intact




nerve cells are not currently available, we used nerve cell synaptosomes




(presynaptic nerve-ending), as  the test system because this fraction




represents a well-characterized and functionally important part of the

-------
neuron.  There Is evidence to show that synaptosomes retain most of the




metabolic and membrane properties of the nerve ending in situ.  As Whittaker




has pointed out, synaptosomes can be regarded as miniature, non-nucleated




neurons, or even as model cells.






Type of Fluorescent Probe Used




     Both intrinsic and extrinsic fluorescent probes were used in these




studies to detect any possible conformational changes.  In these studies, a




fluorochrome, 8-anilino-l-naphthalene sulfonic acid (ANS) was used as an




extrinsic probe since it has been most commonly used in detecting conforma-




tional changes in membranes.  Anesthetics and certain drugs which are known




to act on the cell membrane have been found to cause a change in the ANS




fluorescence in the presence of microsomal, erythrocyte and mitochondrial




membranes.18'19'20'21'22  Spero et al.7reported that tetrodotoxin, a




neurotoxin, reduced the ANS fluorescence increase in guinea pig brain




synaptosomes.




     Fluorescence parameters including (i) fluorescence intensity, (ii)




fluorescence spectra, and (iii) energy transfer from intrinsic membrane




chromophores to ANS were measured to determine if any conformational




changes in the test system had occurred.

-------
                                 SECTION 5




                                  RESULTS






Interaction of ANS with Rat Brain Synaptosomes




     Addition of synaptosomes to a dilute solution of ANS resulted in a




marked enhancement of the fluorescence measured at 490 nm, using light of




390 nm wavelength for excitation.  The enhancement of ANS fluorescence due




to synaptosomes was accompanied by a shift of the emission maximum from




520 to 490 nm wavelength.  Since ANS does not fluoresce in aqueous solution,




the appearance of fluorescence on addition of synaptosomes indicates an




interaction of the dye molecules with synaptosomes.  An enhancement of ANS




fluorescence and a shift of the maximum emission to shorter wavelengths




is characteristic of a change in ANS environment from one of high to low




dielectric constant.  On the basis of the above observations, it is reason-




able to assume that ANS is bound to hydrophobic phase when this compound




interacts with synaptosomes.




     Figure 3 indicates a titration of 6 x 10  M ANS with brain synapto-




somes  (390 nm excitation, 490 nm measurement).  Figure 4 illustrates the




titration of 75 yg/ml of synaptosomal protein/ml with ANS.






Effect of an Acute Dose of DDT on Synaptosome Fluorescence




     In these experiments the effect of DDT was studied  following adminis-




tration of a single dose which produced overt neurological symptoms  in  the




animals.  Sprague-Dawley rats (250-300g) were fasted overnight before being

-------
c
8



I

2
o
3
                        75     100    125


                          Protein (/jg/ml)
175
200
        Figure 3.  Tltration of ANS  (6 x 10~ M) with

                          brain synaptosomes
                               10

-------
c

5
§
                    50
75      100
  ANS(/LiM)
125
150
175
         Figure A.   Titration of brain  synaptosomes
                     (75 yg protein/ml) with ANS
                              11

-------
given high purity UDT in corn oil by oral intubation at a rate of 150 mg/kg


body weight.  Control animals were given corn oil.  The treated animals

showed tremors within 4 hours.  They were then sacrificed by decapitation,

the brain was excised and the synaptosomes were prepared as described

earlier.

     Aliquots of synaptosomal preparation were resuspended in 0.32 M sucrose

in 15 mM Tris-HCl buffer (pH 7.4).  The final membrane concentration was

approximately 75 yg of protein/ml.  An aliquot of ANS stock solution was
                                                          _c
then added to give a final probe concentration of 3.2 x 10  M and fluor-

escence measurements were performed in an Aminco-Keirs spectrofluorometer.

The excitation and emission wavelengths were 390 and 490 nm, respectively.

The emission spectrum of membrane-bound ANS was also measured.



Fluorescence Intensity and Spectra


     The results showed that the fluorescence intensity and spectra of the

ANS bound to synaptosomes from control and DDT-treated rats did not differ.

DDT treatment also caused no change in the fluorescence intensity of ANS

bound to brain mitochondria.  These findings represent the results of three

separate experiments.



Effect of Energy Transfer from Intrinsic Membrane Chromophores to ANS

     The excitation spectrum of ANS overlaps the emission spectrum of

tryptophan and tyroslne.  One might expect a measurable transfer of excita-

tion energy from membrane tryptophane and tyrosine to ANS molecules inserted

in close proximity to these amino acids.  Therefore, in the presence of ANS,

excitation of protein fluorescence by 280 nm light produces energy transfer

from tryptophan emission to bound ANS resulting in ANS fluorescence with an
                                     12

-------
emission peak at about 490 nm.  It has been shown that energy transfer is



sensitive to even a small perturbation in membrane conformation.



     To determine if DDT treatment had an effect on energy transfer, DDT-



exposed or control membrane suspensions (protein content 75 pg/ml) were



placed in cuvettes and the intrinsic protein fluorescence peak  (340 nm) was



read following excitation with 280 nm light.  ANS was then added to the



cuvette and the emission was recorded following excitation at 280 nm.  Treat-



ment with DDT did not cause a change in ANS emission resulting  from excita-



tion at 280 nm, suggesting that the pesticide does not affect the transfer



of tryptophan emission energy to ANS.





Effect of DDT on Calcium-dependent Enhancement in Fluorescence



     The action of DDT on synaptosome-bound ANS fluorescence was further



evaluated by examining the effect of the pesticide on a calcium-dependent


                                                            2+
increase in ANS fluorescence.  Divalent cations including Ca    cause an



increase in the red cell membrane-bound ANS.20'23  It is likely that if



DDT induces any conformational changes in synaptosomes, such changes may


                                             2+                      2+
modify the ANS-fluorescence in response to  Ca  .  We observed that  Ca



enhanced the fluorescence intensity of synaptosome-bound ANS by about  60%.


                                                              2+
When synaptosomes from DDT-treated rats were incubated with Ca   , no change



in fluorescence intensity or  quantum yield  was observed as compared to


                                             2+
untreated synaptosomes also incubated with  Ca





Effect of DDT  on Synaptosomal Protein  (Intrinsic)Fluorescence



     The intrinsic  chromophores of the proteins  in the membrane originate


                                              e\ 1,
from  the amino acids, tyrosine and tryptophan.    A change  in fluorescence



intensity or a shift  in  the position of the peak of intrinsic fluorescence
                                      13

-------
can be used as a measure of conformational changes resulting from treatment


with membrane perturbants.  The intrinsic fluorescence technique has been


used to study the interaction of anesthetics and hormones with erythrocyte

                       n c Of
membranes and proteins.^ '


     For measurement of intrinsic protein fluorescence, the fluorescence


emission was scanned from 300-400 nm following excitation with 280 nm light.


The peak height, which was usually at 340 nm in control synaptosomes was


recorded.  Our results showed that treatment with DDT did not alter the


intensity or emission spectrum of the native protein fluorescence.



Effect of Repeated Doses of DDT on Synaptosomes Fluorescence


     The above studies showed that a single dose of DDT which produced overt


neurological symptoms in rats, did not induce conformational changes in


brain synaptosomes.  Additional studies were undertaken to examine whether


or not administration of repeated sublethal doses of the pesticide to rats


over an extended period induced conformational changes in brain synaptosomes.


     In these studies, two groups of rats (200-250 gm) were given DDT at


two different dosage levels daily for eight consecutive days.  One group


of animals was administered the pesticide daily in corn oil by oral intuba-


tion at a rate of 25 mg/kg body weight.  These experiments were repeated


with the second group using a dose of 50 mg/kg.  Control animals were given


corn oil.  None of the animals in either of the treated groups showed


obvious symptoms of toxicity at the end of the treatment period. They were


then sacrificed by decapitation, the brain was excised and the synaptosomes


were prepared according to the method of Gray and Whittaker.     The effect


of DDT on synaptosomes as measured by extrinsic and intrinsic fluorescence


was determined as described in single-dose studies.


                                     14

-------
     The results showed that like the single dose of DDT, administration of




repeated doses of the pesticide at the. levels used in the study did not




induce any conformational changes in brain synaptosomes as measured by ANS



fluorescence (intensity, emission spectrum and energy transfer).  DDT




treatment also did not alter the intensity or emission spectrum of intrinsic




fluorescence.
Effect of Diphenylhydantoic on Synaptosomal Membranes Exposed to the Drug

in vitro
     Diphenylhydantoic (dilantiir^v is an Important drug used to protect



                                                                         SO
epileptic patients against seizure.  It has been suggested that Dilantin^



interacts with plasma membranes and exerts a stabilizing effect on all




excitable cell membranes.27*28  It was therefore of interest to determine



if the drug induces conformational changes in synaptosomal membranes as




measured by intrinsic and ANS fluorescence.


                                                      fa

     In these studies, the in vitro effect of Dilantiir^ on the fluorescence




of ANS bound to synaptosomes isolated from untreated  rats was examined.



The synaptosomes were incubated with the sodium salt  of diphenylhydantoin




(10~  to 10"  M) for fifteen minutes.  An aliquot of  ANS solution was  then


                                                   _c

added to give a final probe concentration of 5 x 10   M and fluorescence


                                                                          (S)
measurements were made as described above.  We observed that the Dilantin^


                           -4
up to a concentration of 10  M did not cause any change in the fluorescence

                                            •*

intensity or spectrum of ANS.  The chemicals also showed no effect on



intrinsic fluorescence.
                                     15

-------
                                 REFERENCES

 1.   Catton MJ, Harrison MJG, Fullerton PM, et al: Br Med J 2:80, 1970

 2.   Seppalainen AM, Hernberg S: Br J Ind Med 29:243, 1972

 3.   Hilton BD, Bratkowski TA, Yaraada M, et al: Pestic Biochem Physiol
      3:14, 1973

 4.   Hilton BD, O'Brien RD: Pestic Biochem Physiol 3:206, 1973

 5.   Narahashi T: Bull WHO 44:337, 1971

 6.   Segall HJ, Wood JM: Nature 248:456, 1972

 7.   Spero, L, Siemens AJ, Toulis, GA: Mol Pharmacol 9:330, 1973

 8.   Azzi A: Methods Enzymol 32:234, 1974

 9.   Brand L, Gohlke JR: Anna Rev Biochem 41:843, 1972

10.   Chignell CF: Methods in Pharmacology Edited by CF Chignell. 1972,
      2: pp 33

11.   Radda GK: Current Topics in Bioenergetics.  Edited by DR Sanadi.
      1971, 4pp81

12.   Radda GK, Vanderkooi J: Biochim Biophys Acta 265:509, 1972

13.   Seeman P: Pharmacol Rev 24:583, 1972

14.   Gray EG, Whittaker VP: J Anat 96:79, 1962

15.   Lowry OH, Rosebrough NJ, Farr AL, et al: J Biol Chem 193:265, 1951

16.   Whittaker VP, Barker LA: Methods in Neurochemistry.  Edited by
      R Fried. 1972, 2ppl

17.   Narahashi T, Hess HG: J Gen Physiol 51:177, 1968

18.   Azzi A, Chance B, Radda GK, et al: Proc Nat Acad Sci 62:612, 1969

19.   Chance B, Azzi A, Mela L, et al: FEES Lett 3:10, 1969

20.   Feinstein MB, Spero L, Felsenfield: FEBS Lett 6:245, 1971

                                      16

-------
21.   Freedmuu KB, Kadda CK: FEBS Lett 5:150, 1969




22.   Vanderkooi J, Martonosi A: Arch Bloc hem Biophys 133:153, 1969




23.   Rubaclava B, Munoz 1), Gltler C: Biochemistry 8:2742, 1969




24.   Teale FWJ, Weber G: Biochm J 65:476, 1956




25.   Sonnenberg M: Proc Natl Acad Sci USA 68:1051, 1971




26.   Spero L: Proc. Canad Fed Biol Sco 14:32, 1971




27.   O'Donnell JM, Kovacs T, Szabo B: Pflugers Arch 358:275, 1975




28.   Wilensky AJ, Lowden JA: Can J Physiol Pharmacol 50:346, 1972
                                       17

-------
                                   TECHNICAL REPORT DATA
                            (Please read Instructions on the rcrcrse before c
 1. REPORT NO.
  EPA-6QO/1-78-QU
                              2.
                                                           3. RECIPIENT'S ACCESSION-NO.
 4. TITLE AND SUBTITLE

  SCREENING METHODS FOR TOXIC SUBSTANCES
                5. REPORT DATE
                 February 1978
                                                           6. PERFORMING ORGANIZATION CODE
 7. AUTHOR(S)
  Harish  C.  Sikka
                                                           8. PERFORMING ORGANIZATION REPORT NO.
9. PERFORMING ORGANIZATION NAME AND ADDRESS

  Syracuse Research Corporation
  Syracuse, New York 13210
                10. PROGRAM ELEMENT NO.

                    1LA629	
                11. CONTRACT/GRANT NO.

                   68-02-1786
 12. SPONSORING AGENCY NAME AND ADDRESS
  Health Effects  Research Laboratory
  Office of Research and Development
  U.S. Environmental Protection Agency
  Research Triangle Park. N.C. 27711
                                                            13. TYPE OF REPORT AND PERIOD COVERED
RTP.NC
                14. SPONSORING AGENCY CODE

                  EPA 600/11
 15. SUPPLEMENTARY NOTES
 16. ABSTRACT
       The present report deals with  the  application of fluorescent  probe technique
  to the detection of conformational  changes in rat brain synaptosomes  under the
  influence of  certain neurotoxic chemicals, chlorophenothane  (DDT)  and
  diphenylhydantoin, which are expected to produce functional  changes in nerve
  membranes.  Pretreatment of the rats with (i) a single dose  of DDT capable of
  producing neurological symptoms and (ii)  repeated sub-lethal doses of DDT did
  not alter the fluorescence characteristics of the hydrophobic probe 8-anilino-l-
  naphthalene sulfonic acid (ANS) bound to the synaptosomes.   DDT  treatment also showed
  no effect on  native protein fluorescence of synaptosomes.

       Exposure of synaptosomes to diphenylhydantoint in vitro did not  induce
  conformational changes as measured  by ANS and intrinsic fluorescence.
17.
                                KEY WORDS AND DOCUMENT ANALYSIS
                  DESCRIPTORS
                                              b.IDENTIFIERS/OPEN ENDED TERMS
                             c.  COSATI Field/Group
  toxicity
  fluorescent penetration tests
  sieve analysis
  neurochemistry
  brain
  laboratory animals
    toxic substances
    screening  tests
06 A, T
14C
18. DISTRIBUTION STATEMENT
  RELEASE TO PUBLIC
                                              19. SECURITY CLASS (ThisReport}
                                                UNCLASSIFIED
                             21. NO. OF PAGES
                                 23
  20. SECURITY CLASS (Thispage)
     UNCLASSIFIED
                             22. PRICE
EPA Form 2220-1 (9-73)
                                             18

-------