Tissue and Cell 38 (2006) 209–217 Histopathological effects induced by paraquat during Xenopus laevis primary myogenesis P. Mantecca a,∗ , S. Panseri a , R. Bacchetta b , C. Vismara b , G. Vailati b , M. Camatini a a Dipartimento di Scienze dell’Ambiente e del Territorio, Universit` a degli Studi di Milano-Bicocca, 1, Piazza della Scienza, I-20126 Milan, Italy b Dipartimento di Biologia, Universit` a degli Studi di Milano, 26, via Celoria, I-20133 Milan, Italy Received 16 December 2005; received in revised form 21 March 2006; accepted 27 March 2006 Available online 18 May 2006 Abstract The oxidative agent paraquat induced tail abnormalities during Xenopus laevis development. Specimens exposed from blastula to the tadpole stage revealed pear-shaped myocytes and irregular intersomitic boundaries. The histological feature of the axial musculature was evaluated in embryos sampled at significant stages of the primary myogenesis. During the somitogenesis PQ-treated embryos showed normal appearing myotomes, but reduced PAS activity in the post-rotating myotomal cells, and myoblasts with slight vacuolations. Once etched from the vitelline envelope, embryos showed severely altered myoblasts with irregular cellular apexes, heavy sarcoplasmic vacuolations, pyknotic nuclei and disorganizing intersomitic boundaries. Myotomes with many necrotic myocytes containing disorganized contractile material and heavily malformed intersomitic boundaries characterized the late myogenic stages. Our results evidence the heaviest PQ histopathological effects to affect myogenesis of post-etched embryos, suggesting a possible linkage between the swimming activity and the oxidative damage to muscle tissue. © 2006 Elsevier Ltd. All rights reserved. Keywords: X. laevis; Paraquat; Oxidative stress; Myogenesis; Histopathology; Myopathies 1. Introduction The dipyridyl compound paraquat (PQ, 1-dimethyl-4-4 ′ - bypiridylium dichloride) is a non-selective contact herbicide with a broad spectrum of activity, which destroys all green plant tissues (Dodge, 1971). This herbicide can reach water bodies as run-off from agricultural farm lands, but also from direct application in static or slow-moving waters, where it is commonly used at low concentration of 0.1–2 mg/L (Calderbank, 1972), even if sometimes higher concentrations are required. The PQ toxicity mechanism is based on the pro- duction of reactive oxygen species (ROS), in particular the hydroxyl radicals, which cause lipid peroxidation leading to cell death (Dodge, 1971). Thank to its oxidant capacity, PQ is commonly employed in laboratory to study the biologi- cal responses to oxidative damages at cellular and organism ∗ Corresponding author. Tel.: +39 02 64482928; fax: +39 02 64482996. E-mail address: paride.mantecca@unimib.it (P. Mantecca). levels (Melchiorri et al., 1996; Petushok et al., 2002). PQ toxic effects have been widely demonstrated (Haley, 1979; Summers, 1980), and in human PQ has been shown to pro- voke heavy histopathological lesions in lungs and kidneys, sometimes coupled with extensive degeneration and fibrosis of skeletal muscles (Tabata et al., 1999). A study by Vismara et al. (2000) reported the heavy PQ embryotoxicity on Xenopus laevis, coupled with a low teratogenicity level. The LC 50 was 0.138 mg/L and the ter- atogenic index lower than 1. Concentrations near 0.1 mg/L resulted to affect about 30% of the surviving larvae, which showed an abnormal tail flexure. The histological exami- nations of these larvae revealed notochord flexure coupled with abnormal somites, together with vesiculated and pear- shaped myocytes. Vismara et al. (2001) demonstrated that reduced embryotoxic effects were obtained by administering the antioxidant agent ascorbic acid to PQ treated embryos. Together with a clear decrease in the mortality rates, the ascorbic acid diminished the PQ histopathological effects 0040-8166/$ – see front matter © 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.tice.2006.03.002