000162710 001__ 162710 000162710 005__ 20251017144602.0 000162710 0247_ $$2doi$$a10.1016/j.tiv.2025.106132 000162710 0248_ $$2sideral$$a145296 000162710 037__ $$aART-2025-145296 000162710 041__ $$aeng 000162710 100__ $$aGladysz, Aleksandra K. 000162710 245__ $$aStronger prooxidative effects of chromium(VI) comparing to chromium(III) in endocrine and non-endocrine tissues with the thyroid being completely resistant to antioxidant protection 000162710 260__ $$c2025 000162710 5060_ $$aAccess copy available to the general public$$fUnrestricted 000162710 5203_ $$aChromium (Cr) is a harmful heavy metal pollutant. Cr(VI) is a group 1 carcinogen (carcinogenic to humans), whereas Cr(III) is a group 3 carcinogen (not classifiable as to its carcinogenicity to humans). Cr is also documented to be an endocrine disrupting chemical. The study aimed to check whether Cr(VI) compound (K2Cr2O7) or Cr(III) compound (CrCl3·6H2O) induce oxidative damage to membrane lipids (lipid peroxidation, LPO) in homogenates of two endocrine (the thyroid and the ovary) and two non-endocrine (the kidney and the liver) tissues, and whether antioxidants, such as melatonin, indole-3-propionic acid (IPA) and 17β-estradiol, reveal protective effects. Of note, the healthy thyroid gland is characterized by relatively high oxidative stress. Porcine tissue homogenates were incubated in the presence of Cr(VI) (0.05–10.0 mM) or Cr(III) (5.0–200.0 mM) with/without melatonin (5 mM) or IPA (5 mM) or 17β-estradiol (1 mM). The malondialdehyde+4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. Cr(VI) (≥0.1–1.25 mM) significantly increased LPO in all tissues but these damaging effects were not prevented by any antioxidant tested. In turn, Cr(III) (≥25 mM) also significantly increased LPO in all examined tissues. All antioxidants reduced Cr(III)-induced LPO in the ovary, kidney, and liver but had no protective effects in the thyroid. Our findings highlight chromium's strong prooxidative effects, especially in the thyroid. The inability of antioxidants to prevent Cr-induced damage, especially in the thyroid, underscores the need for further research to identify effective protective strategies. 000162710 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttps://creativecommons.org/licenses/by/4.0/deed.es 000162710 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion 000162710 700__ $$aStepniak, Jan 000162710 700__ $$0(orcid)0000-0002-2455-680X$$aLópez-Pingarrón, Laura$$uUniversidad de Zaragoza 000162710 700__ $$aGarcia, Joaquin J. 000162710 700__ $$aKarbownik-Lewinska, Malgorzata 000162710 7102_ $$11012$$2410$$aUniversidad de Zaragoza$$bDpto. Farmac.Fisiol.y Med.L.F.$$cÁrea Fisiología 000162710 773__ $$g110 (2025), 106132$$pToxicol. in vitro$$tTOXICOLOGY IN VITRO$$x0887-2333 000162710 8564_ $$s3606926$$uhttps://zaguan.unizar.es/record/162710/files/texto_completo.pdf$$yVersión publicada 000162710 8564_ $$s2570120$$uhttps://zaguan.unizar.es/record/162710/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada 000162710 909CO $$ooai:zaguan.unizar.es:162710$$particulos$$pdriver 000162710 951__ $$a2025-10-17-14:14:23 000162710 980__ $$aARTICLE