{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T06:25:27Z","timestamp":1791181527369,"version":"4.1.0"},"reference-count":26,"publisher":"SAGE Publications","issue":"7","license":[{"start":{"date-parts":[[1995,7,1]],"date-time":"1995-07-01T00:00:00Z","timestamp":804556800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Hum Exp Toxicol"],"published-print":{"date-parts":[[1995,7]]},"abstract":"<jats:p>\n                    The distribution of the non-selective herbicide paraquat was examined in the brain following subcutaneous admin istration of 20 mg kg\n                    <jats:sup>-1<\/jats:sup>\n                    paraquat ion containing [\n                    <jats:sup>14<\/jats:sup>\n                    C]paraquat to male adult rats in order to determine whether paraquat crosses the blood\/brain barrier. Following administration, [\n                    <jats:sup>14<\/jats:sup>\n                    C]paraquat reached a maxi mal concentration in the brain (0.05% of administered dose) within the first hour and then rapidly disappeared from the brain. However, 24 h after administration of the herbicide, about 13% of the maximal recorded concentra tion of paraquat remained in the brain (1.6 nmol g\n                    <jats:sup>-1<\/jats:sup>\n                    wet weight) and could not be removed by intracardiac perfu sion. Using measurements of [\n                    <jats:sup>14<\/jats:sup>\n                    C]paraquat in dissected brain regions and using quantitative autoradiography we demonstrated an asymmetrical distribution in and around the brain at 30 min (maximal concentration) and 24 h after administration. Most of the paraquat was associated with five structures, two of which, the pineal gland and linings of the cerebral ventricles lie outside the blood\/brain barrier whilst the remaining three brain areas, the anterior portion of the olfactory bulb, hypothalamus and area postrema do not have a blood\/brain barrier. Overall, the distribution of [\n                    <jats:sup>14<\/jats:sup>\n                    C]paraquat in the brain 24 h after systemic administration was highly correlated to the blood volume. These data indicate that any remaining paraquat in the brain 24 h after systemic administration is associated with elements of the cerebro-circulatory sys tem, such as the endothelial cells that make up the capil lary network and that there is a limited entry of paraquat into brain regions without a blood\/brain barrier. No [\n                    <jats:sup>14<\/jats:sup>\n                    C]paraquat was detected in regions where there has been demonstrated pathology in brains from humans with Parkinson's disease. Finally, we could find no evidence for paraquat-induced neuronal cell necrosis 24 or 48 h after systemic administration. Overall it may be concluded that systemically administered paraquat does not pose a direct major neurotoxicological risk in the majority of brain regions which have a functional blood\/brain barrier since paraquat can be excluded from the brain by this barrier.\n                  <\/jats:p>","DOI":"10.1177\/096032719501400706","type":"journal-article","created":{"date-parts":[[2008,12,24]],"date-time":"2008-12-24T01:08:04Z","timestamp":1230080884000},"page":"587-594","source":"Crossref","is-referenced-by-count":46,"title":["Further evidence that the blood\/brain barrier impedes paraquat entry into the brain"],"prefix":"10.1177","volume":"14","author":[{"given":"JL","family":"Naylor","sequence":"first","affiliation":[{"name":"Neurotoxicology Research Group, Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield, Cheshire, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"PS","family":"Widdowson","sequence":"additional","affiliation":[{"name":"Neurotoxicology Research Group, Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield, Cheshire, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"MG","family":"Simpson","sequence":"additional","affiliation":[{"name":"Neurotoxicology Research Group, Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield, Cheshire, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Farnworth","sequence":"additional","affiliation":[{"name":"Neurotoxicology Research Group, Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield, Cheshire, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"MK","family":"Ellis","sequence":"additional","affiliation":[{"name":"Neurotoxicology Research Group, Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield, Cheshire, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"EA","family":"Lock","sequence":"additional","affiliation":[{"name":"Neurotoxicology Research Group, Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield, Cheshire, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[1995,7,1]]},"reference":[{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(86)90495-7"},{"key":"atypb2","first-page":"385","volume":"6","author":"Tiziana M.","year":"1991","journal-title":"Funct Neurol"},{"key":"atypb3","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0773.1992.tb00575.x"},{"key":"atypb4","doi-asserted-by":"publisher","DOI":"10.1016\/0300-483X(73)90029-2"},{"key":"atypb5","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(76)90344-0"},{"key":"atypb6","doi-asserted-by":"publisher","DOI":"10.1016\/0041-008X(80)90138-6"},{"key":"atypb7","doi-asserted-by":"publisher","DOI":"10.1177\/002580249103100111"},{"key":"atypb8","doi-asserted-by":"publisher","DOI":"10.1038\/252314b0"},{"key":"atypb9","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(81)90441-X"},{"key":"atypb10","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(88)90536-9"},{"key":"atypb11","doi-asserted-by":"publisher","DOI":"10.1007\/BF01974345"},{"key":"atypb12","first-page":"243","volume":"2","author":"Hughes JT","year":"1988","journal-title":"Neurotoxicology"},{"key":"atypb13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2559.1980.tb02911.x"},{"key":"atypb14","doi-asserted-by":"publisher","DOI":"10.1016\/0021-9673(93)80578-V"},{"key":"atypb15","doi-asserted-by":"publisher","DOI":"10.1177\/096032719201100616"},{"key":"atypb16","doi-asserted-by":"crossref","first-page":"30","DOI":"10.1016\/S0022-3565(25)27359-1","volume":"153","author":"Glowinski J.","year":"1966","journal-title":"J Pharmacol Exp Ther"},{"key":"atypb17","volume-title":"The Rat Brain in Stereotaxic Coordinates","author":"Paxinos G.","year":"1982"},{"key":"atypb18","first-page":"133","volume":"23","author":"Daniel JW","year":"1966","journal-title":"Br J Ind Med"},{"key":"atypb19","doi-asserted-by":"publisher","DOI":"10.1016\/0041-008X(74)90007-6"},{"key":"atypb20","doi-asserted-by":"publisher","DOI":"10.1016\/0306-3623(77)90045-3"},{"key":"atypb21","first-page":"405","volume":"100","author":"McDowell EM","year":"1976","journal-title":"Arch Path Lab Med"},{"key":"atypb22","doi-asserted-by":"publisher","DOI":"10.1016\/0272-0590(90)90246-G"},{"key":"atypb23","doi-asserted-by":"publisher","DOI":"10.1002\/path.1711210407"},{"key":"atypb24","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(88)90002-X"},{"key":"atypb25","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1990.tb01236.x"},{"key":"atypb26","first-page":"H299","volume":"235","author":"Ohno K.","year":"1978","journal-title":"Am J Physiol"}],"container-title":["Human &amp; 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