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Anatase TiO₂ nanoparticles (NPs) are widely used in food products, capsules, toothpaste, and so on, so the kinds of NPs directly get in touch with human bodies. The potential effect of this kind of material on reproduction must be considered with the increase in infertility. Sixty ICR male mice were intragastrically treated with dosages of 0, 10, 50, and 100 mg kg⁻¹ body weight (BW) anatase TiO₂ NPs to investigate the male reproductive toxicity of the NPs. Sperm quality, morphological changes in mice testes, and oxidative damage indexes were investigated in this study. Results showed that anatase TiO₂ NPs could lead to sperm malformation and increased rate of sperm cell micronucleus. These NPs also reduced the germ cell number and led to spherospermia, interstitial glands vacuole, malalignment, and vacuolization of spermatogenic cells in mice testes. Testicular cells accumulated reactive oxygen species when the mice were intragastrically administrated with TiO₂ NPs. Superoxide dismutase activity decreased, and the malondialdehyde content increased in the TiO₂ NP-treated groups. Anatase TiO₂ NPs exerted potential toxic effects on male reproduction, so the widespread application of this kind of NP in food products needs to be regulated.
The different methyl metabolic products of inorganic arsenic lead to various toxicities. Arsenic has been demonstrated to induce hepatotoxicity by oxidative stress. The relationship between hepatic injury and inorganic methylation is not yet known. This study was designed to explore the relationship between arsenic methylation and liver oxidative stress induced by arsenic trioxide (ATO). Forty healthy KM mice were randomly divided into control group (0.9% saline) and As₂O₃ (1.0 mg/Kg/day, 2.0 mg/Kg/day, 4.0 mg/Kg/day) groups with gastric perfusion for five weeks using high-efficiency liquid chromatography and hydride genesis atomic fluorescence spectroscopy (HPLC-HGAFS). The products of arsenic trioxiode methylating, including trivalent inorganic arsenic (iAs³⁺), pentavalent inorganic arsenic (iAs⁵⁺), mono methyl arsenic (MMA), and dimethyl arsenic (DMA) in the liver were determined. The indexes of arsenic methylation, including primary methyl index (PMI) and second methyl index (SMI) were calculated. The level of hepatic function and activity of MDA, GSH, SOD, and TAOC were detected with kits. We found that the remaining arsenic metabolic products in liver significantly increased with the increasing doses of arsenic trioxide and the liver function and oxidative stress deteriorated. Negative correlations were found between MMA%, PMI and GSH, SOD, and TAOC, while DMA% and SMI positively correlated with the levels of ALT and AST. PMI and SMI negatively correlated with TAOC, GSH, SOD, ALT, and AST, positively linked with the level of MDA. The present study demonstrates that the hepatotoxicity induced by the arsenic accounts for deteriorating oxidative injury activized by arsenic methylation metabolism, providing additional evidence to suggest a mechanism of arsenic poisoning. Therefore, reducing the process of arsenic methylation may be potentially benefical in treating and – more importantly – preventing arseniasis.
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