Abstract

To investigate the response of the tributyltin-degrading fungal strain Cunninghamella elegans to the organotin, a comparative lipidomics strategy was employed using an LC/MS-MS technique. A total of 49 lipid species were identified. Individual phospholipids were then quantified using a multiple reaction monitoring method. Tributyltin (TBT) caused a decline in the amounts of many molecular species of phosphatidylethanolamine or phosphatidylserine and an increase in the levels of phosphatidic acid, phosphatidylinositol and phosphatidylcholine. In the presence of TBT, it was observed that overall unsaturation was lower than in the control. Lipidome data were analyzed using principal component analysis, which confirmed the compositional changes in membrane lipids in response to TBT. Additionally, treatment of fungal biomass with butyltin led to a significant increase in lipid peroxidation. It is suggested that modification of the phospholipids profile and lipids peroxidation may reflect damage to mycelium caused by TBT.

Highlights

  • Organotin compounds have been used as heat stabilizers in PVC, catalysts in chemical reactions, glass coatings, agricultural pesticides, biocides in marine antifoulant paints, wood treatments, and preservatives (Ishihara et al 2012)

  • The increased thiobarbituric acid-reacting substances (TBARS) level found in TBT-treated C. elegans implies the induction of oxidative stress, which results from the imbalance between the generation of reactive oxygen species (ROS) and their removal by the antioxidative system of the cell

  • According to Ishihara et al (2012), the levels of TBARS in the rat organotypic hippocampal slices treated with TBT were approximately three times higher than those in untreated slices

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Summary

Introduction

Organotin compounds have been used as heat stabilizers in PVC, catalysts in chemical reactions, glass coatings, agricultural pesticides, biocides in marine antifoulant paints, wood treatments, and preservatives (Ishihara et al 2012). Tributyltin (TBT) is reported to be immuno-, neuro-, hepato-, nephro-, and gastrotoxic and it causes testicular damage (Gupta et al 2011). The mechanism(s) by which TBT induces toxicity have not been fully established. Liu et al (2008) reported that the organotin induced oxidative damage to mice cells both in vivo and in vitro. Oxidative stress, which results from the overproduction of reactive oxygen species (ROS), causes cellular oxidative injury such as lipid peroxidation, protein oxidation, and DNA damage (Ishihara et al 2012). According to Chahomchuen et al (2009), TBT induced apoptosis in Saccharomyces cerevisiae , which was associated with ROS production. TBT altered lipids homeostasis by disturbing fatty acids composition (Bernat and Długoński 2007, 2012)

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