Oxidative metabolism in the cardiorespiratory system after an acute exposure to nickel-doped nanoparticles in mice

GARCÉS, MARIANA; MARCHINI, TIMOTEO; CÁCERES, LOURDES; CALABRÓ, VALERIA; MEBERT, ANDREA M.; TUTTOLOMONDO, MARÍA VICTORIA; VICO, TAMARA; VANASCO, VIRGINIA; TESAN, FIORELLA; SALGUEIRO, JIMENA; ZUBILLAGA, MARCELA; DESIMONE, MARTÍN F.; VALACCHI, GIUSEPPE; ALVAREZ, SILVIA; MAGNANI, NATALIA D.; EVELSON, PABLO A.

TOXICOLOGY

ELSEVIER IRELAND LTD

Año: 2021

0300-483X

There is an increasing concern over the harmful effects that metallic nanoparticles (NP) mayproduce on human health. Due to their redox properties, nickel (Ni) and Ni-containing NP areparticularly relevant. Hence, the aim of this study was to establish the toxicological mechanismsin the cardiorespiratory oxidative metabolism initiated by an acute exposure to Ni-doped-NP.Mice were intranasally instilled with silica NP containing Ni (II) (Ni-NP) (1 mg Ni (II)/kg bodyweight) or empty NP as control, and 1h after exposure lung, plasma, and heart samples wereobtained to assess the redox metabolism. Results showed that, NP were mainly retained in thelungs triggering a significantly increased tissue O2 consumption rate, leading to Ni-NP-increasedreactive oxygen species production by NOX activity, and mitochondrial H2O2 production rate.In addition, an oxidant redox status due to an altered antioxidant system showed by lungGSH/GSSG ratio decreased, and SOD activity increased, resulting in an increased phospholipidoxidation. Activation of circulating polymorphonuclear leukocytes, along with GSH/GSSG ratiodecreased, and phospholipid oxidation were found in the Ni-NP-group plasma samples.Consequently, in distant organs such as heart, Ni-NP inhalation alters the tissue redox status.Our results showed that the O2 metabolism analysis is a critical area of study following Ni-NPinhalation. Therefore, this work provides novel data linking the redox metabolisms alterationselicited by exposure to Ni (II) adsorbed to NP and cardiorespiratory toxicity.