Mechanisms of kidney toxicity for chromium- and arsenic-based preservatives: Potential involvement of a pro-oxidative pathway

• CCA causes damages in renal tubules, with the possible involvement of oxidative mechanisms.
• Among CCA components, arsenic and chromium exert strong modifications on antioxidant defence.
• Oxidative stress biomarkers are increased, following CCA, arsenic and chromium exposures.

Metals have been extensively used for the preservation of wood. Among metallic conservatives, mixtures of chromated copper arsenate (CCA) were thoroughly used. However, the release and consequent mobilization of such compounds by biota, may culminate in the exertion of toxic chemical effects. The present study intended to show the toxicological effects caused by arsenic (7.2 mg/kg body weight), chromium (10.2 mg/kg Cr body weight) and the commercial mixture CCA (7.2 mg/kg As body weight and 10.2 mg/kg Cr body weight) in mice, namely the oxidative stress response (catalase – CAT, glutathione peroxidase – GPx, and glutathione-S-transferases – GSTs), in kidney tissues. The determination of the tested parameters was performed after exposure; organisms were exposed, and then sacrificed at two distinct periods, namely 14 and 96 h after the administration of toxicants. Exposure to chromium and arsenic induced significant modifications in the redox state of the test organisms, evidenced by significant alterations in GSTs and GPx activities. No alterations were found concerning the activity of catalase. These findings showed that the chemical mixture used as household product may exert significant toxicological outcomes in exposed animals, such as rodents, conditioning their redox homeostasis and antioxidant response.