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ToxSci Advance Access published online on December 2, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfh025
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
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Received September 12, 2003; accepted October 29, 2003
© 2003 Society of Toxicology

System Toxicology

Comparative Study on Cardiotoxic Effect of Tinuvin 770: A Light Stabiliser of Medical Plastics in Rat Model

Péter Sótonyi 1*, Béla Merkely 2, Márta Hubay 3, Jenõ Járay 1, Endre Zima 2, Pál Soós 2, Anikó Kovács 4, and István Szentmáriay 3

1 Department of Transplantation and Surgery, Semmelweis University, Budapest, Hungary, 1082
2 Department of Cardiovascular Surgery, Semmelweis University, Budapest, Hungary, 1122
3 Department of Forensic Pathology, Semmelweis University, Budapest, Hungary, 1091
4 National Institute of Forensic Toxicology, Budapest, Hungary, 1146

* To whom correspondence should be addressed. E-mail: sotonyi{at}hotmail.com.


  Abstract

Tinuvin 770/bis(2,2,6,6-tetramethyl-4-piperidinyl) sebacate, is a UV light stabiliser plastic additive used world-wide. It is a component of many plastic materials used in medical and food industries. Earlier studies demonstrated its in-vitro L-type Ca2+ channel and nicotinic acetylcholine receptor blocking properties. Our previous experiments have proved the toxic effects of Tinuvin 770 on isolated rat cardiomyocytes.

The present study investigates the cardiotoxic effects of Tinuvin 770 in vivo.

Wistar rats were intraperitoneally injected with increasing doses of Tinuvin 770/1, 10, 100 [mu]g, 1 mg/for fifteen times during a five-week period. Myocardial samples were analysed by light-, electron, and fluorescent microscopy. Lead-acetate method was used to detect intracellular Ca2+, and glyoxylic acid technique to assess alteration in adrenergic innervation. Focal myocytolysis and hypercontraction necrosis could be observed in rats treated with higher doses of Tinuvin 770. In these groups, intracellular Ca2+ accumulation and increased catecholamine release were detected. Tinuvin 770 does not only display L-type Ca2+ channel blocking properties, but can also lead to catecholamine release, similar to effects of first generation of L-type Ca2+ channel blockers. Morphological results correspond to catecholamine induced myocardial damage. Current literature as well as our study indicates that more detailed toxicological analysis of Tinuvin 770 should be required and current regulations in medical and food industries should adopt the new results.

Key Words: Tinuvin 770, cardiotoxicity, catecholamine, L-type Ca2+ channels, light-stabilisers, haemodialysis .


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