Dermal exposure to nano-TiO2 induced cardiovascular toxicity through oxidative stress, inflammation and apoptosis

Qian Zhang; Zhimin Liu; Junting Du; Wei Qin; Manman Lu; Haiyan Cui; Xiaoxiao Li; Shumao Ding; Rui Li; Junlin Yuan

doi:10.2131/jts.44.35

Original Article

Dermal exposure to nano-TiO₂ induced cardiovascular toxicity through oxidative stress, inflammation and apoptosis

Qian Zhang, Zhimin Liu, Junting Du, Wei Qin, Manman Lu, Haiyan Cui, Xiaoxiao Li, Shumao Ding, Rui Li, Junlin Yuan

Author information

Qian Zhang
Laboratory of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, China
Zhimin Liu
Laboratory of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, China
Junting Du
Laboratory of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, China
Wei Qin
Laboratory of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, China
Manman Lu
Laboratory of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, China
Haiyan Cui
Laboratory of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, China
Xiaoxiao Li
Laboratory of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, China
Shumao Ding
Laboratory of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, China
Rui Li
Laboratory of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, China
Junlin Yuan Corresponding author
Laboratory of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, China

Keywords: Nano-titanium dioxide (nano-TiO₂), Cardiovascular toxicity, Oxidative stress, Inflammation, Cytotoxicity, Apoptosis

JOURNAL FREE ACCESS FULL-TEXT HTML

2019 Volume 44 Issue 1 Pages 35-45

DOI https://doi.org/10.2131/jts.44.35

Details

Abstract

Due to its excellent properties such as ultraviolet obscuration, chemical stability and small particle size, nano-titanium dioxide (nano-TiO₂) is widely used, particularly in sunblock products. The skin is therefore a chief route for exposure. Studies have found that oral or respiratory exposure to nano-TiO₂ has an adverse impact on the cardiovascular system. The relationship between dermal exposure to nano-TiO₂ and cardiovascular system toxicity, particularly the causative mechanisms, remain unclear. In this study, we used Balb/c mice to evaluate cardiovascular toxicity from nano-TiO₂ dermal exposure, and the underlying mechanisms associated with the human umbilical vein endothelial cells (HUVECs) were explored. Our results showed that nano-TiO₂ treatment resulted in an obvious increase in reactive oxygen species and 8-hydroxy-2’-deoxyguanosine, indicating the appearance of oxidative stress. Moreover, the levels of inflammatory biomarkers, such as immunoglobulin E, soluble intercellular adhesion molecule-1, interleukin-8, and hypersensitive C-reactive protein, also increased. Exposing HUVECs to nano-TiO₂ led to a decline in cell vitality, and an increase in caspase-3 levels, suggesting that nano-TiO₂ exposure caused cytotoxicity and even cell apoptosis. Interestingly, neutralizing oxidative stress by administering Vitamin E was shown to reduce the inflammatory response and cytotoxicity. Our findings suggest that nano-TiO₂ can injure the cardiovascular system via dermal exposure, and does this via oxidative stress-induced inflammation and cytotoxicity. Vitamin E treatment may be a strategy to mitigate the damage.

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