Synthetic Musks Fragrances In The Aquatic
Environment: In Vitro Toxicological Studies Of
Their Biotransformation And
Potential Negative Effects
Author(s)
S. Focardi, C. Della Torre, M. Monti, T. Biagini & I. Corsi
Abstract
The aim of the present study was to investigate the interaction of musk xylene
(MX) and Tonalide (AHTN) with CYP1A by looking at gene transcription
(cyp1a) and EROD activity in Poeciliopsis lucida hepatoma cell line (PLHC-1).
MX and AHTN were studied individually and combined with classical inducer
of CYP1A as B(a)P and PCB126. After 24h of exposure a different cytotoxicity
has been observed with an LC50 of 35.76μM for AHTN and LC50 123.6μM for
MX. After 6h of exposure to MX, a dose-dependent reduction of cyp1a was
observed respect to controls. At 24h, the same pattern was observed but with
slight induction at the lowest concentration (2μM) and a dose-dependent
reduction at the higher concentrations. Co-exposure to MX with B(a)P did not
alter cyp1a transcription levels compared to the inducer alone. After 6h AHTN
determined a slight induction of cyp1a transcription reaching maximum
induction of 2.3 folds respect to controls at 2μM. No modulation of cyp1a
transcription was observed after 24h. Co-exposure to AHTN with B(a)P and
PCB126 at 6h determined a 55% reduction of cyp1a transcription respect to
inducers alone which recovered at 24h. At 24h, MX caused a dose-dependent
decrease of EROD activity. No modulation of EROD activity was detectable at
6h and 24h of exposure to AHTN. Co-exposure with both MX and AHTN did
not alter EROD activity induced by B(a)P and PCB126. Results suggest different
toxicological properties of MX and AHTN toward CYP1A in PLHC-1. MX
reduced cyp1a basal transcription but did not alter cyp1a induction by B(a)P and
PCB126. This suggests that MX cellular pathway is not mediated by AhR. On
Keywords
synthetic musks, PLHC-1, CYP1A
Related Book
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