Toxicology Letters 187 (2009) 63–68 Contents lists available at ScienceDirect Toxicology Letters journal homepage: www.elsevier.com/locate/toxlet Effects of 3,3  ,4,4  ,5-pentachlorobiphenyl (PCB126) on vertebral bone mineralization and on thyroxin and vitamin D levels in Sprague–Dawley rats Pedro Alvarez-Lloret a , P. Monica Lind b , Ingrid Nyberg c , Jan Örberg c , Alejandro B. Rodríguez-Navarro a,∗ a Departamento de Mineralogía y Petrología, Facultad de Ciencias, Universidad de Granada, Avenida Fuentenueva s/n, 18071 Granada, Spain b Institute of Environmental Medicine, Division of Biochemical Toxicology, Karolinska Institutet, Box 210, S-171 77 Stockholm, Sweden c Uppsala University, Department of Environmental Toxicology, Norbyvägen 18 A, S-752 36 Uppsala, Sweden article info Article history: Received 14 September 2008 Received in revised form 16 January 2009 Accepted 20 January 2009 Available online 7 February 2009 Keywords: PCB126 Bone mineral density TEM FTIR Vitamin D Thyroxin abstract The aim of the present study is to use Fourier transform infrared spectrometry (FTIR), and transmission electron microscopy (TEM) techniques, to make a more detailed description of toxic effects of 3,3  ,4,4  ,5- pentachlorobiphenyl (PCB126) on bone tissue at the microstructural and at the molecular level as a result of an altered bone metabolism. We have analysed potential changes on vitamin D and thyroxin serum levels since these hormones represent endocrine endpoints that are critical for bone growth and devel- opment. For this purpose Sprague–Dawley rats were exposed (n =10) to PCB126 (i.p.) for 3 months (total dose, 384 g/kg bodyweight), while control rats (n =10) were injected with corn oil (vehicle). Results from FTIR showed that vertebrae from the exposed rats had an overall lower degree of mineralization (−8.5%; p < 0.05) compared with the controls. In addition, results from peripheral quantitative computed tomography (pQCT) analyses showed significant increases in the trabecular bone mineral density (+12%; p <0.05) in the exposed group compared with the controls. The TEM analyses also showed an alteration in the crystallinity properties of vertebral bone mineral with a significant decrease in the size and crys- tallinity of apatite crystal forming the bone tissue in the exposed vs. non-exposed rats. Serum analysis revealed lower levels of thyroid hormones, FT4 (−42%; p < 0.005), TT4 (−26%; p < 0.005), and vitamin D (−21%; p < 0.005) in exposed group compared to control animals. The complementary techniques (TEM and FTIR) used in this study have revealed insights into possible bone mineralization alteration due to PCB126 exposure. The lowering of both the thyroxin and vitamin D serum levels might be an underlying explanation for the observed effects on bone mineralization. © 2009 Elsevier Ireland Ltd. All rights reserved. 1. Introduction Polychlorinated biphenyls (PCBs) are widespread and persistent organic pollutants (POPs). PCBs were widely used as diluents, flame retardants, fluids for capacitors and transformers (Hansen, 1999). A group of PCB congeners, the so-called dioxin-like PCBs, includ- ing 3,3  ,4,4  ,5-pentachlorobiphenyl (PCB126), can assume a planar configuration similar to that of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The presence and bioaccumulation of PCB in biota and in the environment have been extensively described (Tanabe, 1988; Hoffman et al., 1996; Kannan et al., 1998; Magnusson et al., 2006). Several studies have reported toxic effects due to PCB exposure in animals and in vitro experimental systems. In animals, this exposure to PCBs might cause a variety of adverse effects, including hepatic microsomal-enzyme induction, liver enlargement, lipid deposition, necrosis, higher serum levels of liver-associated enzymes, fibrosis ∗ Corresponding author. E-mail address: anava@ugr.es (A.B. Rodríguez-Navarro). or carcinogenicity (US EPA, 1996). Previous findings in experimental animal studies show that the development and homeostasis of bone tissue is negatively affected after exposure to dioxins and dioxin- like compounds (Hermsen et al., 2008; Jämsä et al., 2001; Lind et al., 2004; Lundberg et al., 2007; Miettinen et al., 2005; Ramajayam et al., 2007). Moreover, epidemiological studies regarding humans indicate a relationship between exposure to POPs and impaired bone tis- sue homeostasis (Glynn et al., 2000; Hodgson et al., 2008; Wallin et al., 2004). Similarly, mounting evidence indicates that exposure to POPs can alter bone tissue homeostasis also in free-ranging ani- mals (Bengtsson et al., 1985; Bergman et al., 1992; Lind et al., 2003; Lundberg et al., 2007; Olsson et al., 1994; Rodriguez-Navarro et al., 2006; Sonne et al., 2004). Bone, looked at a microstructural level, is a biocomposite con- sisting basically of apatite crystals deposited in an oriented fashion and integrated within an organic matrix, mostly collagen fibrils (Boskey, 2007). Bone remodelling (i.e. bone resorption and for- mation) is essential to skeletal-bone renewal and for maintaining normal calcium homeostasis. This so-called bone remodelling is 0378-4274/$ – see front matter © 2009 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.toxlet.2009.01.030