Tioacetamid – frakcja wdychana : dokumentacja proponowanych dopuszczalnych wielkości narażenia zawodowego

Bruchajzer, Elżbieta; Szymańska, Jadwiga; Frydrych, Barbara

doi:10.5604/01.3001.0013.6380

Artykuł - szczegóły

Tytuł artykułu

Tioacetamid – frakcja wdychana : dokumentacja proponowanych dopuszczalnych wielkości narażenia zawodowego

Autorzy

Bruchajzer Elżbieta , Szymańska Jadwiga , Frydrych Barbara

Treść / Zawartość

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Identyfikatory

DOI

10.5604/01.3001.0013.6380

Warianty tytułu

Thioacetamide – inhalable fraction : documentation of proposed values of occupational exposure limits (OELs)

Języki publikacji

Abstrakty

Tioacetamid występuje w postaci bezbarwnych kryształów o charakterystycznym zapachu merkaptanów. Dawniej był stosowany jako: fumigant zapobiegający gniciu pomarańczy, środek przyspieszający wulkanizację gumy oraz stabilizator oleju napędowego. Obecnie jest wykorzystywany w analizie jakościowej jako źródło siarkowodoru. Według informacji z Centralnego Rejestru Danych o Narażeniu na Substancje, Mieszaniny, Czynniki lub Procesy Technologiczne o Działaniu Rakotwórczym lub Mutagennym w latach 2005-2016 w Polsce na tioacetamid narażonych było od 486 do 1 137 osób. Większość z nich stanowiły kobiety. Wartość LD50 po dożołądkowym podaniu związku szczurom wynosi 301 mg/kg mc. Tioacetamid ma silne działanie hepatotoksyczne. Tioacetamid podany szczurom w pojedynczej dawce powodował martwicę zrazików wątrobowych. Podawany wielokrotnie prowadził do uszkodzenia wątroby, o czym świadczyły m.in. zmiany biochemiczne (zwiększenie aktywności: aminotransferaz, gamma-glutamylotransferazy, alkalicznej fosfatazy oraz stężenia bilirubiny w surowicy), a także jej marskość. Skutki toksycznego działania tioacetamidu wykazane w doświadczeniach przewlekłych na zwierzętach świadczą o wyraźnej zależności ich występowania od czasu narażenia. Po przewlekłym narażeniu szczurów na tioacetamid w wodzie do picia (o stężeniu 0,03%, czyli około 35 mg/kg mc./dzień) lub w paszy (0,5% w paszy, czyli około 28 mg/kg mc./dzień) po 4 miesiącach notowano zapalenie wątroby i miejscowe ogniska martwicy w wątrobie, później zmiany te nasilały się, a po 8 ÷ 17 miesiącach występowały: przewlekłe zapalenie wątroby, marskość oraz nowotwory wątroby i przewodów żółciowych. Wyniki badań mutagenności i genotoksyczności tioacetamidu nie są jednoznaczne. Można przyjąć, że związek stwarza ryzyko uszkodzenia materiału genetycznego w warunkach in vivo, po biotransformacji do silnie hepatotoksycznego metabolitu. Przemiany metaboliczne tioacetamidu w organizmie prowadzą – w wyniku S-oksydacji, głównie przy udziale CYP2E1 – do sulfotlenku (TASO), a następnie hepatotoksycznego, bardzo reaktywnego sulfonu (TASO2). Ma on podstawowe znaczenie w mechanizmie działania toksycznego związku (łącząc się z makrocząsteczkami wątroby). Metabolity tioacetamidu nasilają także stres oksydacyjny. Wystąpienie nowotworów w przewlekłych eksperymentach na zwierzętach spowodowało, że Międzynarodowa Agencja Badań nad Rakiem (IARC) w 1987 roku zaliczyła tioacetamid do grupy 2B, czyli do czynników przypuszczalnie rakotwórczych dla człowieka. Zgodnie z klasyfikacją CLP eksperci Unii Europejskiej zaliczyli tioacetamid do substancji rakotwórczych kategorii zagrożenia 1B z przypisem H350 „może powodować raka”. Za podstawę wyznaczenia wartości najwyższego dopuszczalnego stężenia (NDS) przyjęto hepatotoksyczne działanie tioacetamidu na szczury, którym podawano związek wielokrotnie drogą dożołądkową. Za wartość NDS zaproponowano stężenie 1,5 mg/m3 . Nie ma podstaw do wyznaczenia wartości najwyższego dopuszczalnego stężenia chwilowego (NDSCh) oraz dopuszczalnego stężenia w materiale biologicznym (DSB). Zaproponowano także oznaczenie związku „Carc. 1B” informujące, że jest to substancja rakotwórcza kategorii zagrożenia 1B. Zakres tematyczny artykułu obejmuje zagadnienia zdrowia oraz bezpieczeństwa i higieny środowiska pracy będące przedmiotem badań z zakresu nauk o zdrowiu oraz inżynierii środowiska.

Thioacetamide occurs in the form of colorless crystals with a characteristic smell of mercaptans. It was used in the past as a fumigant to prevent oranges from rotting, in rubber vulcanization and as a diesel stabilizer. It is currently used in a qualitative analysis as a source of hydrogen sulfide. According to information from the Central Register of Data on Exposure to Carcinogenic or Mutagenic Substances, Mixtures, Factors or Technological Processes in 2005-2016 from 486 to 1137 people were exposed to thioacetamide in Poland. Most of them were women. The LD50 value after intragastric administration of the compound to rats is 301 mg/kg. Thioacetamide is a strong hepatotoxic agent, its single dose caused hepatic necrosis. Administered repeatedly it induced liver damage, which was indicated by biochemical changes and cirrhosis. The effects of thioacetamide toxicity in chronic animal experiments indicated a relationship to exposure time. After chronic exposure of rats to thioacetamide in drinking water (at 0.03%, i.e., approximately 35 mg/kg/day) or in feed (0.5% in feed, i.e., approximately 28 mg/kg/day), hepatitis and local hepatic foci were noted after 4 months, these changes later intensified, and after 8–17 months chronic hepatitis, cirrhosis and cancer of the liver and bile ducts occurred. The results of mutagenicity and genotoxicity studies of thioacetamide are inconclusive. It can be assumed that the compound may damage genetic material in vivo after biotransformation to a highly hepatotoxic metabolite. The metabolism of thioacetamide by S-oxidation (mainly with the participation of CYP2E1) leads to the production of sulfoxide (TASO), and then to hepatotoxic, highly reactive sulfone (TASO2). The latter is of fundamental importance for the mechanism of toxic action of thioacetamide (by binding with hepatic macromolecules). Thioacetamide metabolites also induce oxidative stress. Because of neoplasms observed in chronic studies, International Agency for Research on Cancer (IARC) included thioacetamide in group 2B – agents probably carcinogenic to humans. According to the CLP classification, thioacetamide is a category-1B carcinogen with a “H350 – May cause cancer” note. The hepatotoxic effects of thioacetamide in rats after repeated administration were used as the basis for determining the maximum acceptable concentration (MAC; TLV-TWA – threshold limit value-time weighted average). A concentration of 1.5 mg/m3 was proposed as the MAC value. There are no bases to determine the short-term exposure limit (STEL) and the biological limit value (BLV). “Carc. 1B” marking is also proposed, as thioacetamide is a category-1B carcinogen. This article discusses the problems of occupational safety and health, which are covered by health sciences and environmental engineering.

Słowa kluczowe

tioacetamid narażenie zawodowe toksyczność NDS inżynieria środowiska nauki o zdrowiu

thioacetamide occupational exposure toxicity MAC-TWA environmental engineering health sciences

Wydawca

Centralny Instytut Ochrony Pracy - Państwowy Instytut Badawczy

Czasopismo

Podstawy i Metody Oceny Środowiska Pracy

Rocznik

2019

Tom

Nr 4 (102)

Strony

149--179

Opis fizyczny

Bibliogr. 108 poz., rys., tab.

Twórcy

autor

Bruchajzer Elżbieta

elzbieta.bruchajzer@umed.lodz.pl

Uniwersytet Medyczny w Łodzi 90-151 Łódź, ul. J. Muszyńskiego 1 POLAND

autor

Szymańska Jadwiga

Uniwersytet Medyczny w Łodzi 90-151 Łódź, ul. J. Muszyńskiego 1 POLAND

autor

Frydrych Barbara

Uniwersytet Medyczny w Łodzi 90-151 Łódź, ul. J. Muszyńskiego 1 POLAND

Bibliografia

1. Abbasi M.H., Akhtar T., Malik I.A., Farima S., Khawar B., Mujeeb K.A., Mustafa G., Hussain S., Iqbal J., Sheikh N. (2013). Acute and chronic toxicity of thioacetamide and alteration in blood cell indices in rats. J. Cancer Therapy 4, 251–259.
2. Abdalla O., Elboshy M., Risha E., Mohammed F.H., Abu G.W. (2016). Hepatoprotective and antioxidant effects of pomegranate against thioacetamide toxicicty in rats. Ann. Vet. Anim. Sci. 3(1), 28–41.
3. Abdel Salam O.M.E., Mohammed N.A., Sleem A.A., Farrag A.R. (2013). The effect of antidepressant drugs on thioacetamide-induced oxidative stress. Eur. Rev. Med. Pharmacol. Sci. 17, 735–744.
4. Abul H., Mathew T.C., Dashti H.M., Al-Bader A. (2002). Level of superoxide dismutase, glutathione peroxidase and uric acid in thioacetamide-induced cirrhotic rats. Anal. Histol. Embryol. 31, 66–71.
5. Ackerman Z., Pappo O., Link G., Glazer M., Grozovski M. (2015). Liver toxicity of thioacetamide is increased by hepatocellular iron overload. Biol. Trace Elem. Res. 163, 169–176.
6. Ahmed H.H., Saeed R.M.A., Sayed A.A., Achmed Y.S. (2014). Update on pathophysiologic mechanizms of thioacetamide-induced hepatic encephalopathy. World J. Pharm. Pharmaceut. Sci. 3(12), 138–167.
7. Akhtar T., Sheikh N. (2013). An overview of thioacetamide-induced hepatotoxicity. Toxin Rev. 32(3), 43–46.
8. Al-Attar A.M., Al-Rethea H.A. (2016). Chemoprotective effect of omega-3 fatty acids on thioacetamide induced hepatic fibrosis in male rats. Saudi J. Biol. Sci. 18(11). e4784; doi: 10.1779/zjrms-4781.
9. Amacher D.E., Turner G.N. (1982). Mutagenic evaluation of carcinogens and non-carcinogens in the L5178Y/TK assay utilizing postmitochondrial fractions (S9) from normal rat liver. Mutat. Res. 97, 49–65 [cyt. za: Arni 1989].
10. Ambrose A.M., deEds F., Rather L.J. (1949). Toxicity of thioacetamide in rats. J. Ind. Hyg. Toxicol. 31(3), 159–161.
11. Amer M.G., Mazen N.F., Mohamed A.M. (2017). Caffeine intake decreases oxidative stress and inflammatory biomarkers in experimental liver diseased induced by thioacetamide: biological and histological study. Int. J. Immunopathol. Pharmacol. 30(1), 12–24.
12. Anghileri L.J., Heidbreder M., Weiler G., Dermietel R. (1977). Hepatocarcinogenesis by thioacetamide: correlations of histological and biochemical changes and possible role of cell injury. Exp. Cell. Biol. 45, 34–47.
13. Arni P. (1989). Review on the genotoxic activity of thioacetamide. Mutat. Res. 221(2), 153–162.
14. Arni P., Müller D. (1986). Automated microbial mutagenicity testing with Cobas Bact. Mutat. Res. 164, 287–288 [cyt. za: Arni 1989].
15. Augustine M.L., Poulasen N.K., Heinze J.E. (1982). Evaluation of the CHO/HGPRT cell mutation test using 12 compounds. Environ. Mutagen. 4, 389–390 [cyt. za: Arni 1989].
16. Barker E.A., Smuckler E.A. (1974). Nonhepatic thioacetamide injury. II. Morphologic features of proximal renal tubular injury. Am. J. Pathol. 74(3), 575–590.
17. Bastway M., Hasona N.A., Abdel Hamid H. (2008). Effects of zinc acetate on thioacetamide-induced hepatotoxicity in rats. Bull. Egypt Soc. Physiol. Sci. 28(2), 81–89.
18. Becker F. (1983). Thioacetamide hepato carcinogenesis. J. Natl. Cancer Inst. 71(3), 553–558.
19. Breau A.P., Mitchell W.M., Karkhanis D.W., Field L. (1984). Thiono compounds: 3. chemical oxidation of thioacetamide to a mutagenic S-oxide. Mutat. Res. 139, 1–4 [cyt. za: Arni 1989].
20. CCRIS (2018). Chemical Carcinogenisis Research Information System. Thioacetamide, CASRN: 62-5-55 [dostęp: 20.07.2018; komputerowa baza danych].
21. Chanda S., Mangipudy R.S., Warbritton A., Bucci J., Mehendale H.M. (1995). Stimulated hepatic tissue repair underlies hepatoprotection by thioacetamide against acetaminophen-induced lethality. Hepatology 21(2), 477–486.
22. ChemIDplus (2018). Thioacetamide. A Toxnet database [dostęp: 12.02.2018; komputerowa baza danych toksykologicznych].
23. Chen T.M., Subeq Y.M., Lee R.P., Chiou T.W., Hsu B.G. (2008). Single dose intravenous thioacetamide administration as a model of acute liver damage in rats. Int. J. Exp. Path. 89, 223–231.
24. Chieli E., Aliboni M., Saviozzi M., Malvaldi G. (1987). Introduction of micronucleated erythrocytes by primary thioamides and their metabolites in the mouse. Mutat. Res. 192, 141–143 [cyt. za: Arni 1989].
25. Chilakapati J., Shankar K., Korrapati MC., Hill R.A., Mehandale H.M. (2005). Saturation toxocokinetics of thioacetamide: role in initiation of liver injury. Drug Metabol. Disp. 33(12), 1877–1885.
26. Craddock V.M., Henderson A.R. (1978). De novo and repair replication of DNA in liver of carcinogen-treated animals. Cancer Res. 38, 2135–2143 [cyt. za: Arni 1989].
27. Cruz A., Padillo F.J., Torres E., Navarrete C.M., Munoz-Castaneda J.R., Caballero F.J., Briceno J., Marchal T., Tunez I., Montilla P., Pera C. Muntane J. (2005). Melatonin prevents experimental liver cirrhosis induced by thioacetamide in rats. J. Pineal Res. 39, 143–150.
28. CzynRak (2018). Czynniki rakotwórcze – informacje z Centralnego Rejestru Danych o Narażeniu na Substancje, Mieszaniny, Czynniki lub Procesy Technologiczne o Działaniu Rakotwórczym lub Mutagennym. Łódź, Instytut Medycyny Pracy.
29. Dasgupta A., Chatterjee R., Choudhury J.R. (1981). Thioacetamide induced hepatocarcinoma in rat. Oncology 38(4), 249–253.
30. De Flora S. (1981). Study of 106 organic and inorganic compounds in the Salmonella/microsome test. Carcinogenesis 2(4), 283–298 [cyt. za: Arni 1989].
31. De Flora S., Zanacchi P., Camairano A., Bennicelli C., Badolati G.S. (1984). Genotoxic activity and potency of 135 compounds in the Ames revision test and in a bacterial DNA-repair-test. Mutat. Res. 133, 161–198 [cyt. za: Arni 1989].
32. Diala E., Mittwoch U., Wilkie D. (1980). Antimitochondrial effects of thioacetamide and ethylenethiourea in human and yeast cell cultures. Br. J. Cancer 42, 112 [cyt. za: Arni 1989].
33. Dunkel V.C., Zeiger E., Brusick D., McCoy E., McGregor D., Mortelmans K., Rosenkranz H.S., Simmon V.F. (1984). Reproducibility of microbial mutagenicity assay: I. Tests with Salmonella typhimurium and Escherichia coli using a standardized protocol. Environ. Mol. Mutagen. 6 (Suppl. 2), 1–254 [cyt. za: CCRIS 2018].
34. ECHA (2018) [https://echa.europa.eu/pl/brief-profile/-/briefprofile/100.000.493].
35. Egilsson V., Evans I.H., Wilkie D. (1979). Toxic and mutagenic effects of carcinogens on the mitochondria of Saccharomyces cerevisiae. Mol. Gen. Gente. 174, 39–46 [cyt. za: Arni 1989].
36. Fahrat K., Grasedyck K., Lindner J., Schütte B., Okpanyi S.N., Eurich R. (1979). Rat liver collagen in protracted thioacetamide poisoing. Part 4. Determination of collagen-like protein (CLP) and hydroxyproline content in the serum as a parameter of disturbed liver collagen metabolism. Arzneimittelforschung 29(1), 82–90 [cyt. za: HSDB 2018].
37. Fitzhugh O.G., Nelson A.A. (1948). Liver tumors in rats fed thiourea and thioacetamide. Science 108, 626–628.
38. Fluck E.R., Poirier L.A., Ruelius H.W. (1976). Evaluation of a DNA polymerase-deficient mutation of E. coli for the rapid detection of carcinogens. Chem. Biol. Inteact. 15, 219–231 [cyt. za: Arni 1989].
39. Fontana L., Moreira E., Torres M.I., Fernandez M.I., Rios A., Sanchez de Medina F., Gil A. (1996). Serum amino acid changes in rats with thioacetamide-induced liver cirrhosis. Toxicology 106, 197–206.
40.Furtado K.S., Prado M.G., Aguiare Silva M.A., Dias MC., Rivelli D.P., Rodrigues M.A.M., Barbisan L.F. (2012). Coffee and caffeina protect against liver injury induced by thioacetamide in male Wistar rats. Basis Clin. Pharmacol. Toxicol. 111, 339–347.
41. Ghosh S., Sankar A., Bhattacharyya S., Sil P.C. (2016). Silymarin protects mouse liver and kidney from thioacetamide induced toxicity by scavenging reactive oxygen species and activating PI3K-akt pathway. Front. Pharmacol. 7, 481. Doi: 10.3389/fphar.2016.00481.
42. Gothoskar S.V., Talwalkar G.V., Bhide S.V. (1970). Tumorigenic effect of thioacetamide in Swiss strain mice. Br. J. Cancer 24(3), 498–503.
43. Gupta D.N. (1955). Production of cancer of bile ducts with thioacetamide. Nature 175(4449), 257.
44. Gupta D.N. (1956). Nodular cirrhosis and metastasising tumours produced in the liver of rats by prolonged feeding with thioacetamide. J. Path. 72(2), 415–426.
45. Hajovsky H., Hu G., Koen Y., Sarma D., Cui W., Moore D.S., Staudinger J.L., Hanzlik R.P. (2012). Metabolizm and toxicity of thioaacetamide and thioacetamide oxide in rat hepatocytes. Chem. Res. Toxicol. 25(9), 1955–1963.
46. Hayes S., Gordon A., Sadowski I., Hayes C. (1984). Rkbacterial test for independently measuring chemical toxicity and mutagenicity: short-term forward selection assay. Mutat. Res. 130, 97–106 [cyt. za: Arni 1989].
47. HSDB (2018). Hazardous Substances Data Bank. N-Nitrosodimethylamine. National Library of Medicine, Bethseda, Maryland 2017 [komputerowa baza danych; dostęp: 2018.07.25].
48. Hussein S.A., Elhadary A.E.A., Elgzar Y.M. (2014). Biochemical study on the protective effect of curcumin on thioacetamide induced hepatotoxicity in rats. Benha Vet. Med. J. 27(1), 175–185.
49. IARC (1974). Monographs on the evaluation on the carcinogenic risk of chemicals to humans. Some anti-thyroid and related substances, nitrofurans and industrial chemicals. IARC, Lyon. Tioacetamide Vol. 7, 77–83.
50. IARC (1987). IARC Monographs on the evaluation of carcinogenic risk to humans. WHO, International Agency for Research on Cancer, Vol. 1–42, Suppl. 7.
51. IARC (2018). List of classification [Klasyfikacja czynników rakotwórczych wg Miedzynarodowej Agencji Badań nad Rakiem]. Agents classified by IARC Monographs, Vol. 1–122.
52. Ichinotsubo D., Mower H.F., Setliff J., Mandel M. (1977). The use of rec-bacteria for testing of carcinogenic substances. Metat. Res. 46, 53–62 [cyt. za: Arni 1989].
53. Jeong E.S., Kim G., Jung Shin H., Park S.M., Oh J.H., Kim Y.B., Moon K.S., Choi H.K., Jeong J., Shin J.G., Kim D.H. (2015). Increased serum bile acid concentration following low-dose chronic administration of thioacetamide in rats, as evidenced by metabolomic analysis. Toxicol. Appl. Pharmacol. 288, 213–222.
54. Kabiri N., Ahanger-Darabi M., Setorki M., Raeian-Kopaei M. (2013). The effect of silimarin on liver injury by thioacetamide in rats. J. Herb. Med. Pharmacol. 2(2), 29–33.
55. Kang J.S., Wanibuchi H., Morimura K., Wongpoomchai R., Chusiri Y., Gonzalez F.J., Fukushima S. (2008). Role of CYP2E1 in thioacetamide-induced mouse hepatotoxicity. Toxicol. Appl. Toxicol. 228, 295–300.
56. Kawachi T., Komatsu T., Kada T., Ishidate M., Sasaki M., Sugiyama T., Tazima Y. (1980). Results of recent studies on the relevance of various short-term screening tests in Japan. Appl. Meth. Oncol. 3, 253–267 [cyt. za: Arni 1989].
57. Kawai H., Ishibashi T., Kudo N., Kawashima Y., Mitsumoto A. (2012). Behavioral and biochemical characterization of rats treated chronically with thioacetamide: proposal of an animal model for hepaticenceohalopathy associated with cirrhosis. J. Toxicol. Sci. 37(6), 1165–1175.
58. Khawar M.B., Abbasi M.H., Fatima S., Mujeeb K.A., Sheikh N. (2016). Alteration in proteins and transaminases activity induced by thioacetamide in albino rats. Punjab. Univer. J. Zool. 31(2), 269–276.
59. Korsund G.O., Grice H.G., Goodman T.K., Knipfel J.E., McLaughlan J.M. (1973). Sensitivity of several serum enzymes for the detection of thioacetamide, dimethylnitrosamine and diethanoloamine – induced liver damage in rats. Toxicol. Appl. Pharmacol. 26, 299–313.
60. Kuroda K., Terao K., Akao M. (1987). Inhibitory effect of fumaric acid on hepatocarcinogenesis by thioacetamide In rats. J. Natl. Cancer Inst. 79, 1047–1051 [cyt. za: Hajovsky i in. 2012].
61. Lewis R.J. (2004). Sax’s dangerous properties of industrial materials. 11th ed., Vol. 3, Willey Interscience, A John Wiley & Sons, Inc. Publication, 2709–2710.
62. Li J.F., Chen B.C., Lai D.D., Jia Z.R., Andersson R., Zhang B., Yao J.G., Yu Z. (2011). Soy isoflavone delays the progression of thioacetamide-induced liver fibrosis in rats. Scand. J. Gastroenterol. 46, 341–349.
63. Maini M.M., Stich H.F. (1961). Chromosomes of tumor cells. II. Effect of various liver carcinogens on mitosis of the Escherichia coli K12 inductest for detection of potential chemical carcinogens. Mutat. Res. 130, 141–151 [cyt. za: Arni 1989].
64. Mangipudy R.S., Chanda S., Mehandale H.M. (1995a). Tissue repair response as a function of dose in thioacetamide hepatotoxicity. Environ. Health Perspect. 103, 260–267.
65. Mangipudy R.S., Chanda S., Mehendale H.M. (1995b). Hepatocellular regeneration: key to thioacetamide autoprotection. Pharmacol. Toxicol. 77(3), 182–188.
66. McCann J., Choi E., Yamasaki E., Ames B.N. (1975). Detection of carcinogens as mutagens in the Salmonella/microsomes test: assay of 300 chemicals. Part I. Proc. Natl. Acad. Sci. (UAS) 72(12), 5135–5139 [cyt. za: Arni 1989].
67. Mirkova E.T. (1996). Activities of the rodent carcinogens thioacetamide and acetamide in the mouse bone marrow micronucleus assay. Mutat. Res. 352, 23–30.
68. Mironescu S. (1969). Mitotic abnormalities in proliferating hepatocytes induced by thioacetamide at certain periods after partial hepatectomy. Exptl. Cell Res. 55, 435–437 [cyt. za: Arni 1989].
69. Mironescu S. (1970). Nucleolar and mitotic alterations induced by thioacetamide in regenerating hepatocytes at different periods after partial hepatectomy. Int. Cancer Congr. Agstracts 10, 317 [cyt. za: Arni 1989].
70. Mironescu S., Burducea O., Sahanazarov N. (1969). Nucleolar and mitotoxic abnormalieties produced by thioacetamide and hydroxylamine in monkey kidney cells cultivated in vitro. Exptl. Cell. Res. 57, 193–204 [cyt. za: Arni 1989].
71. Mironescu S., Ciovirnache M. (1971). Mitotic, chromosomal and nucleolar alterations induced by thioacetamide in relation to the mitotic cycle after partial hepatectomy. J. Natl. Cancer Inst. 46, 49–61 [cyt. za: Arni 1989].
72. Mironescu S., Encut I., Mironescu K., Licui F. (1968). Nucleolar behavior in regenerating liver of rats receiving intra-abdominal injections of azo dyes and thioacetamide. J. Natl. Cancer Inst. 40, 917–933 [cyt. za: Arni 1989].
73. Mitchell A.D., Rudd C.J., Caspary W.J. (1988). Evaluation of the L5178Y mouse lympoma cell mutagenesis assay: intralaboratory results for sixty-three coded chemicals tested at SRI International. Environ. Mol. Mutagen. 12(13), 37–101 [cyt. za: Arni 1989].
74. Müller A., Machnik F., Zimmermann T., Schubert H. (1988). Thioacetamide-induced cirrhosis – like liver lesions in rats – usefulness and reliability of this animal model. Exp. Pathol. 34(4), 229–236.
75. Munoz Torres E., Paz Bouza J.P., Lopez Bravo A., Abad Hernandez M.M., Carrascal Marino E. (1991). Experimental thioacetamide-induced cirrhosis of the liver. Histol. Histopathol. 6, 95–100.
76. Mustafa H.N., Al Awdan S.A., Hegazy G.A. (2013). Protective role of antioxicants on thiocetamide-induced acute hepatic encephalopathy: biochemical and ultrastructural study. Tissue and Cell 45, 350–362.
77. Myhr B.C., Caspary W.J. (1988). Evaluation of L5178Y mouse lymphoma cell mutagenesis assay: intralaboratory results for sixty-three coded chemicals tested at Litton Bionetics, Inc. Environ. Mol. Mutagen. 12(13), 103–194 [cyt. za: Arni 1989; CCRIS 2018].
78. Nakamura S., Oda Y., Shimada T., Oki I., Sugimoto K. (1987). SOS-inducing activity of chemical carcinogens and mutagens in Salmonella typhimurium TA1535/pSK 1002: examination with 151 chemicals. Mutat. Res. 192, 239–246 [cyt. za: Arni 1989].
79. Nygaard O., Eldjarn L., Nakken K.F. (1954). Studies on the metabolism of thioacetamide-S35 in the intact rat. Cancer Res. 14, 625–628.
80. Oda Y., Nakamura S., Oki I., Kato T., Makino K., Nakata A., Shinagawa H. (1984). A simple test system (Umu-test) for the detection of environmental mutagens. II. Improvement of sensitivity by employing salmonella typhimurium TA1535 as a host strain. Mutat. Res. 130, 375 [cyt. za: Arni 1989].
81. Oda Y., Nakamura S., Oki I., Kato T., Shinagawa H. (1985). Evaluation of the New system (Umu-test) for the detection of environmental mutagens and carcinogens. Mutat. Res. 147, 219–229 [cyt. za: Arni 1989].
82. Okigaki T. (1976). Thioacetamide-induced changes in diploid cultures of human liver. Proc. Jpn. Acad. 52, 195–198 [cyt. za: Arni 1989].
83. Paes D., Thompson S. (1979). Forward mutagenesis as a test system in Salmonella typhimurium. Mutat. Res. 64, 119–120 [cyt. za: Arni 1989].
84. Preat M.M., Roels H.J. (1984). Histogenesis of cholangiomas and cholangiocarcinomas in thioacetamide fed rats. Exp. Pathol. 26(1), 3–14.
85. Rees K.R., Rowland G.F., Varcie J.S. (1966). The metabolism of tritiated thioacetamide in the rat. Int. J. Cancer 1(2), 197–206.
86. RoC, Raport on Carcinogens (2016). 14th ed. Thioacetamide CAS No. 52-55-5. National Toxicology Program, Department of Health and Human Services.
87. Rosenkranz H.S., Poirier L.A. (1979). Evaluation of the mutagenicity and DNA-modifying activity of carcinogens and noncarcinogens in microbial systems. J. Natl. Cancer Inst. 62, 873–892 [cyt. za: Arni 1989].
88. Rozporządzenie Parlamentu Europejskiego i Rady (WE) Nr 1272/2008 z dnia 16 grudnia 2008 r. w sprawie klasyfikacji, oznakowania i pakowania substancji i mieszanin, zmieniają- ce i uchylające dyrektywy 67/548/EWG i 1999/45/WE oraz zmieniające rozporządzenie (WE) nr 1907/2006. Dz. Urz. UE L 353 z dnia 31.12.2008 [Regulation (EC) No 1272/2008 of the European Parliament and of the Council of 16 December 2008 on classification, labelling and packaging of substances and mixtures, amending and repealing Directives 67/548/ EEC and 1999/45/EC, and amending Regulation (EC) No 1907/2006].
89. RTECS, Registry of Toxic Effects of Chemical Substances (2018). Thioacetamide. National Institutes for Occupational Safety and Health, Cincinnati, Ohio.
90. Shank R.C., Barrows L.R. (1981). Toxicity-dependent DNA methylation: significance to risk assessment, health risk analysis. Proc. 3rd Life Science Symposium 1980. Chapter 18, 225–235 [cyt. za: Arni 1989].
91. Silva de Miranda A., Rodrigues D.H., Vieira L.B., Lima C.X., Alvarenga Rachid M., Vieira Teixeira Vidigal P., Gomez M.V., dos Reis H.J., Guatimosim C., Teixeira A.L. (2010). A thioacetamide-induced hepatic encephalopathy model in C57BL/6 mice. Arq. Neuropsiquiatr. 66(4), 597–602.
92. Simmon V.F. (1979). In vitro mutagenicity assays of chemical carcinogens and related compounds with Salmonella Typhimurium. J. Natl. Cancer Inst. 62, 893–899 [cyt. za: Arni 1989].
93. Sirag H.M. (2007). Biochemical studies on thioacetamide toxicity in male albino rats and the role of tomato juice as an antioxi dant. Mansoura J. Forensic Med. Clin. Toxicol. 15(2), 99–114.
94. Sui H., Matsumoto H., Wako Y., Kawasako K. (2015). Evaluation of in vivo genotoxicity by thioacetamide in a 28-day repeated-dose liver micronucleus assay using male young adult rats. Mutat. Res. 780–781, 81–84.
95. Tanaka E., Terada M., Misawa S. (2000). Cytochrome P450 2E1: its clinical and toxicological role. J. Clin. Pharm. Ther. 25, 165–175 [cyt. za: Chilakapati i in. 2005].
96. Terraccini B., Della Porta G. (1961). Feeding with aminoazo dyes, thioacetamide and ethionine. Arch. Path. 71, 566–575.
97. The Merck Index (2001). An encyclopedia of chemicals, drugs, and biologicals. [Ed.] M.J. O’Neil. 13th ed. Whitehouse Station, NJ, Merck and Co., Inc. , 1189.
98. Thioacetamide T:0430 (2017). [Ed.] R.P. Pohanish [In:] Sittig’s handbook of toxic and hazardous chemicals and carcinogens. 7th ed. William Andrew, Elsevier, Oxford, UK, Cambridge, US.
99. Topham J.C. (1980). Do induced sperm-head abnormalities in mice specifically identify mammalian mutagens rather than carcinogens? Mutat. Res. 74, 379–387 [cyt. za: Arni 1989].
100. Trennery P.N., Waring R.H. (1983). Early changes in thioacetamide – induced liver damage. Toxicol. Lett. 19(3), 299–307.
101. Watanabe K., Sasaki T. Kawakami K. (1998). Comparison of chemically-induced mutation among four bacterial strains, Salmonella Typhimurium TA102 and TA2638, and Escherichia coli WP2/PKM101 and WP2 UVRA/PKM101: collaborative study III and evaluation of the usefulness of these strains. Mutat. Res. 416(3), 169–181 [cyt. za: CCRIS 2018].
102. Waters N.J., Waterfield C.J., Farrant R.D., Holmes E., Nicholson J.K. (2005). Metabonomic deconvolution of embedded toxicity: application to thioacetamide hepato- and nephrotoxicity. Chem. Res. Toxicol. 18, 639–654.
103. Wilkie D., Gooneskera S. (1980). The yeast mitochondrial system in carcinogen testing. Chem. Industr. (London) 21, 847– 850 [cyt. za: Arni 1989].
104. Yeh C.N., Maitra A., Lee K.F., Jan Y.Y., Chen M.F. (2004). Thioacetamide-induced intestinal-type cholangiocarcinoma in rat: an animal model recapitulating the multi-stage progression of human cholangiocarcinoma. Carcinogenesis 25, 631-636 [cyt. za: Hajovsky i in. 2012].
105. Zamani N., Naghsh N., Fathpour H. (2014). Comparing poisonous effects of thioacetamide and silver nanoparticles on enzymatic changes and liver tissue in mice. Zahedan J. Res. Med. Sci. 16(2), 54–57.
106. Zargar S., Wani T.A., Alamro A.A., Ganaie M.A. (2017). Amelioration of thioacetamide-induced liver toxicity in Wistar rats by rutin. Int. J. Immunopathol. Pharmacol. 30(3), 207–214.
107. Zimmerman T., Müller A., Machnik G., Franke H., Schubert H., Dargel R. (1987). Biochemical and morphological studies on production and regression of experimental liver cirrhosis induced by thioacetamide in Uje: Wist rats. Z. Versuchstierkd. 30, 165–180.
108. Zimmermann T., Franke H., Dargel R. (1986). Studies on lipid and lipoprotein metabolism in rat liver cirrhosis induced by different regimens of thioacetamide administration. Exp. Pathol. 30, 109–117.

Uwagi

Opracowanie rekordu w ramach umowy 509/P-DUN/2018 ze środków MNiSW przeznaczonych na działalność upowszechniającą naukę (2019).

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Bibliografia

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