Influence of Different Sizes of Titanium Dioxide Nanoparticles on Hepatic and Renal Functions in Rats with Correlation to Oxidative Stress

Abstract

As titanium dioxide (TiO(2)) nanoparticles are widely used commercially, the potential effects of TiO(2) nanoparticles on humans are a concern. To evaluate the effects of TiO(2) nanoparticles on hepatic and renal functions and correlate changes to oxidative stress, Sprague-Dawley rats were treated with TiO(2) particles of two different specific surface areas (TiO(2-S50): 50 m(2)/g, and TiO(2-S210): 210 m(2)/g) at 0.5, 5, or 50 mg/kg body weight by intratracheal instillation. After 7 d, TiO(2) nanoparticles produced no obvious acute toxicity on hepatic and renal functions. However, superoxide dismutase (SOD) activity of plasma and glutathione peroxidase (GSH-PX) activity of kidney in the low-dose TiO(2-S210) group were significantly decreased. After TiO(2-S210) exposure, malondialdehyde (MDA) levels of liver and kidney in intermediate and high-dose groups were significantly increased. This change only appeared in liver after TiO(2-S50) exposure. Furthermore, SOD activity in liver and kidney and GSH-PX activity in kidney with low TiO(2-S210) exposure group were significantly less than with low TiO(2-S50). No apparent pathological changes in liver and kidney were observed. Intratracheal exposure to TiO(2) nanoparticles may induce oxidative stress in liver and kidney, but does not influence hepatic or renal functions. There was no apparent evidence that TiO(2-S210) was more toxic than TiO(2-S50). In general, intratracheal exposure to TiO(2) did not markedly affect extrapulmonary tissue functions.

General and Electrophysiological Toxic Effects of Manganese in Rats following Subacute Administration in Dissolved and Nanoparticle Form

“…A similar effect of NPs on the liver was seen also previously (with Mn NPs: Oszlánczi et al [13]; but also with Cd NPs: Horváth et al [22]). The dependence of the effect more on the nanoparticulate character than on the chemical composition is supported by literature data on in vivo liver damage related to oxidative stress in rats treated with intratracheal TiO 2 NPs [23], and oxidative damage of in vitro human hepatic cells on exposure to ZnO NPs [24]. The decreased body weight gain in rats exposed to Mn NPs (oral + intratracheal treatment: groups MnL33 and MnH33) is also an indication of stress (as suggested in [25]) especially in combination with the increased weight of the adrenals in these groups (see Tables 2 and 3).…”

Linoleic acid suppresses colorectal cancer cell growth by inducing oxidant stress and mitochondrial dysfunction

“…The levels of MDA and the activity of SOD, the biomarkers of oxidative stress, were measured as described previously with commercial reagent kits purchased from Nanjing Kaiji Bioengineering Institute (Nanjing, China) [19]. The cell MDA content and SOD activity were also represented as corresponding value:…”

Oxidative stress studies of six TiO2and two CeO2nanomaterials: Immuno-spin trapping results with DNA

“…Table III summarizes several experimental studies of oxidative stress and literature reviews of TiO 2 exposures, health effects and carcinogenicity studies performed by individual research groups, IARC or NIOSH. There are several citations of nanomaterialinduced increases in thiobarbituric acid reactive substances (TBARS) in mouse skin and liver (Wu et al 2009), mouse kidney and liver (Liang et al 2009), carp gill, liver and brain (Hao et al 2009) and trout gill, brain and intestine (Federici et al 2007). In a comparative study of TiO 2 and hematite nanomaterials in human lung BEAS-2B and/or IMR-90 cells, a TiO 2 nanomaterial (Degussa~91 nm) exposure caused an increase in acellular electron spin resonance signals with the spin trap molecule DMPO, increased cellular fluorescence from 2¢,7¢-dichlorodihydrofluorescein diacetate and increased cellular 8-hydroxydeoxyguanosine concentration as determined by an ELISA kit (Bhattacharya et al 2009).…”