Hepatic megalocytosis due to vanadium inhalation: participation of oxidative stress

Abstract

The aim of this study was to evaluate the morphological changes, liver function test (LFT), and oxidative stress damage caused by thiobarbituric acid reactive substances (TBARS), in mice exposed to vanadium via inhalation. Male CD-1 mice were exposed to vanadium pentoxide (V(2)O(5)) via inhalation (0.02 M), 1 hour twice a week for 6 weeks. At the end of the protocol, controls and exposed mice were killed to evaluate the changes. Histological analysis and LFT were performed to detect the damage. TBARS detection was assessed for oxidative stress. Inflammatory infiltration, binucleation, and meganucleus were detected in the liver of V(2)O(5)-exposed mice (p < 0.05). Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were also significantly increased (p < 0.05). Lipid peroxidation was significantly higher in V(2)O(5)-exposed animals compared to controls (p < 0.05). V(2)O(5) exposure induced inflammation and cell damage detected by the increase in ALT and AST levels, as well as histological changes that suggest regenerative changes, such as binucleation and meganucleus.

The Effect of Atmospheric Pollution on the Thymus

“…In brief, V-inhalation decreased the thymic CD11C+ and MHCII+ cells as the exposure time increased [4]. An explanation for our findings could be the V-oxidative capacity which has been previously reported by our group and by other authors [34,35]. Oxidative stress could affect the liberation of pro-inflammatory transcription factors by the CD11c cells.…”

Vanadium pentoxide increased PTEN and decreased SHP1 expression in NK-92MI cells, affecting PI3K-AKT-mTOR and Ras-MAPK pathways

“…PTEN intracellular increase dephosphorylates membrane PIP2 and PIP3 (Leslie et al 2016), thus inactivating the Akt and mTOR signaling pathway (GarciaJunco-Clemente and Golshani, 2014); as the results showed. V 2 O 5 is known to induce an intracellular oxidative environment (Cano-Gutierrez et al 2012) and such an environment inhibits the activity of PTEN, promoting the accumulation of proteins (Matsumoto et al 2016). This mechanism can explain the increase in PI3K and phosphorylated PI3K.…”

CD11c decrease in mouse thymic dendritic cells after vanadium inhalation

“…To explain the modification in CD11c presence, we make use of the V potential to induce oxidative stress in our model reported by us and other authors (Gusik et al, 2003;Cano-Gutierrez et al, 2011). Oxidative stress liberates reactive oxygen (ROS) and nitrogen species (NOS) that may modify pro-inflammatory transcriptional factors and could modify the expression of CD11c.…”