Tinuvin 770 [bis(2,2,6,6-tetramethyl-4-piperidinyl) sebacate], is a UV light stabilizer
plastic additive used worldwide. 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 microg, and 1 mg) 15 times during a 5-week period. Myocardial samples were analyzed by light, electron, and fluorescent microscopy. The
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 not only displays L-type Ca2+ channel blocking properties, but can also lead to
catecholamine release, similar to effects of the 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.