Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 2.1
5-Year Impact Factor – 2.2
Scopus CiteScore – 3.4 (CiteScore Tracker 3.4)
Index Copernicus  – 161.11; MEiN – 140 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
Periodicity – monthly

Download original text (PL)

Advances in Clinical and Experimental Medicine

2006, vol. 15, nr 4, July-August, p. 677–681

Publication type: review article

Language: Polish

Ftalany – budowa, działanie, znaczenie kliniczne

Phthalates – Structure, Activity, Clinical Meaning

Kinga Belowska−Bień1,, Zygmunt Zdrojewicz2,

1 Klinika Chorób Wewnętrznych, Zawodowych i Nadciśnienia Tętniczego AM we Wrocławiu

2 Klinika Endokrynologii, Diabetologii i Leczenia Izotopami AM we Wrocławiu

Streszczenie

Ftalany są czynnikami toksycznymi wobec procesów rozwoju i rozmnażania u zwierząt. Są powszechnie używane jako plastyfikatory w produkcji materiałów opartych na PCV i środków medycznych: opakowań preparatów krwi, urządzeń do hemodializy, zgłębników nosowo−żołądkowych i innych. Podejrzewa się, że ftalany zakłócają funkcję układu wewnątrzwydzielniczego, szczególnie przez efekt estrogenopodobny. Ekspozycja na ftalany samców szczurów w czasie życia płodowego powoduje zmiany w obrębie jąder analogiczne do zespołu dysgenetycznego u ludzi. Ftalany powodują spadek stężenia insuliny i kortyzonu w surowicy krwi oraz zawartości glikogenu w wątrobie, a także wzrost stężenia glukozy we krwi oraz T3 i T4 w surowicy. Suplementacja witaminy E zapobiega szkodliwym efektom indukowanym przez ftalany u samic szczurów.

Abstract

Phthalates are developmental and reproductive toxicants in animals. They are widely used as plasticizers in the manufacture of PVC−based materials and medical devices: blood bags, hemodialysis tubing, nasogastric feeding tubes, and others. Phthalates are suspected to disrupt the endocrine system, especially through estrogenic effects. Fetal exposure of male rats to some phthalates induces testicular changes similar to testicular dysgenesis syndrome in humans. Phthalates induce decrease in serum insulin, cortisol and liver glycogen and increase in blood glucose, serum T3 and T4. Vitamin E administration prevents phthalate−induced harmful effects in female rats.

Słowa kluczowe

ftalany

Key words

phthalates

References (26)

  1. Brown D, Thompson RS: Chemosphere 1982, 11, 4, 427.
  2. Brossa L, Marce RM, Borrull F, Pocurull E: Occurrence of twenty−six endocrine−disrupting compounds in environmental water samples from Catalonia, Spain. Environ Toxicol Chem 2005, 24, 2, 261–267.
  3. Klamer HJ, Leonards PE, Lamoree MH, Villerius LA, Kerman JE, Bakker JF: A chemical and toxicological profile of Dutch North Sea surface sediments. Chemosphere 2005, 58, 11, 1579–1587.
  4. Hulls AG: Determination of the effects of Vestinol AH (DEHP) on the survival and reproduction of Daphnia magna. Final Report No DL−160, 1995.
  5. Wang Y, Hu W, Cao Z, Fu X, Zhu T: Occurrence of endocrine−disrupting compounds in reclaimed water from Tianjin. Bioanal Chem. 2005, 383, 5, 857–863.
  6. Kurahashi N, Kondo T, Omura M, Umemura T, Ma M, Kishi R: The effects of subacute inhalation of di−(2− ethylhexyl) phthalate (DEHP) on the testes of prepubertal Wistar rats. J Occup Health 2005, 47, 5, 437–444.
  7. Takeuchi S, Iida M, Kobayashi S, Jin K, Matsuda T, Kojima H: Differential effects of phthalate esters on transcriptional activities via human estrogen receptors alpha and beta, and androgen receptor. Toxicology 2005, 1, 210, 2–3, 223–233.
  8. Lee SK, Veeramachaneni DN: Subchronic exposure to low concentrations of di−n−butyl phthalate disrupts spermatogenesis in Xenopus laevis frogs. Toxicol Sci 2005, 84, 2, 394–407.
  9. Akingbemi BT, Ge R, Klinefelter GR, Zirkin BR, Hardy MP: Phthalate−induced Leydig cell hyperplasia is associated with multiple endocrine disturbances. Proc Natl Acad Sci USA 2004, 20, 101, 3, 775–780.
  10. Stroheker T, Cabaton N, Nourdin G, Regnier JF, Lhuguenot JC, Chagnon MC: Evaluation of anti−androgenic activity of di−(2−ethylhexyl)phthalate. Toxicology 2005, 1, 208, 1, 115–121.
  11. Borch J, Ladefoged O, Hass U, Vinggaard AM: Steroidogenesis in fetal male rats is reduced by DEHP and DINP, but endocrine effects of DEHP are not modulated by DEHA in fetal, prepubertal and adult male rats. Reprod Toxicol 2004, 18, 1, 53–61.
  12. Gayathri NS, Dhanya CR, Indu AR, Kurup PA: Changes in some hormones by low doses of di (2−ethylhexyl) phthalate (DEHP), a commonly used plasticizer in PVC blood storage bags & medical tubing. Indian J Med Res 2004, 119, 4, 139–144.
  13. McKinnell C, Sharpe RM, Mahood K, Hallmark N, Scott H, Ivell R, Staub C, Jegou B, Haag F, Koch−Nolte F, Hartung S: Expression of insulin−like factor 3 protein in the rat testis during fetal and postnatal development and in relation to cryptorchidism induced by in utero exposure to di (n−Butyl) phthalate. Endocrinology 2005, 146, 10, 4536–4544.
  14. Wilson VS, Lambright C, Furr J, Ostby J, Wood C, Held G, Gray LE Jr.: Phthalate ester−induced gubernacular lesions are associated with reduced insl3 gene expression in the fetal rat testis. Toxicol Lett 2004, 2, 146, 3, 207–215.
  15. Thompson CJ, Ross SM, Gaido KW: Di(n−butyl) phthalate impairs cholesterol transport and steroidogenesis in the fetal rat testis through a rapid and reversible mechanism. Endocrinology 2004, 145, 3, 1227–1237.
  16. Wyde ME, Kirwan SE, Zhang F, Laughter A, Hoffman HB, Bartolucci−Page E, Gaido KW, Yan B, You L: Di−n−butyl phthalate activates constitutive androstane receptor and pregnane X receptor and enhances the expression of steroid−metabolizing enzymes in the liver of rat fetuses. Toxicol Sci 2005, 86, 2, 281–290.
  17. Ortiz−Zarragoitia M, Cajaraville MP: Effects of selected xenoestrogens on liver peroxisomes, vitellogenin levels and spermatogenic cell proliferation in male zebrafish. Comp Biochem Physiol C Toxicol Pharmacol 2005, 141, 2, 133–144.
  18. Lee KY, Shibutani M, Takagi H, Kato N, Takigami S, Uneyama C, Hirose M: Diverse developmental toxicity of di−n−butyl phthalate in both sexes of rat offspring after maternal exposure during the period from late gestation through lactation. Toxicology 2004, 15, 203, 1–3, 221–238.
  19. Hong EJ, Ji YK, Choi KC, Manabe N, Jeung EB: Conflict of estrogenic activity by various phthalates between in vitro and in vivo models related to the expression of Calbindin−D9k. J Reprod Dev 2005, 51, 2, 253–263.
  20. Seidlova−Wuttke D, Jarry H, Wuttke W: Pure estrogenic effect of benzophenone−2 (BP2) but not of bisphenol A (BPA) and dibutylphtalate (DBP) in uterus, vagina and bone. Toxicology 2004, 1, 205, 1–2, 103–112.
  21. Fan LQ, You L, Brown−Borg H, Brown S, Edwards RJ, Corton JC: Regulation of phase I and phase II steroid metabolism enzymes by PPAR alpha activators. Toxicology 2004, 15, 204, 2–3, 109–121.
  22. Shipley JM, Waxman DJ: Simultaneous, bidirectional inhibitory crosstalk between PPAR and STAT5b. Toxicol Appl Pharmacol 2004, 15, 199, 3, 275–284.
  23. Dhanya CR, Gayathri NS, Mithra K, Nair KV, Kurup PA: Vitamin E prevents deleterious effects of di (2−ethyl hexyl) phthalate, a plasticizer used in PVC blood storage bags. Indian J Exp Biol 2004, 42, 9, 871–875.
  24. Duty SM, Calafat AM, Silva MJ, Ryan L, Hauser R: Phthalate exposure and reproductive hormones in adult men. Hum Reprod 2005, 20, 3, 604–610.
  25. Jonsson BA, Richthoff J, Rylander L, Giwercman A, Hagmar L: Urinary phthalate metabolites and biomarkers of reproductive function in young men. Epidemiology 2005, 16, 4, 487–493.
  26. Rais−Bahrami K, Nunez S, Revenis ME, Luban NL, Short BL: Follow−up study of adolescents exposed to di(2− −ethylhexyl) phthalate (DEHP) as neonates on extracorporeal membrane oxygenation (ECMO) support. Environ Health Perspect 2004, 112, 13, 1339–1340.