TiO2 nanoparticles potentiated the cytotoxicity, oxidative stress and apoptosis response of cadmium in two different human cells

• Published in: Environmental science and pollution research international Vol. 27; no. 10; pp. 10425 - 10435
• Main Authors: Ahamed, Maqusood, Akhtar, Mohd Javed, Alaizeri, ZabnAllah M., Alhadlaq, Hisham A.
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01-04-2020; Springer Nature B.V
• Subjects: Antioxidants; Apoptosis; Aquatic Pollution; Atmospheric Protection/Air Quality Control/Air Pollution; Bcl-2 protein; Breast cancer; Cadmium; Catalase; Cytotoxicity; Depletion; Earth and Environmental Science; Ecotoxicology; Environment; Environmental Chemistry; Environmental Health; Environmental science; Gene expression; Glutathione; Glutathione reductase; Hydrogen peroxide; Internalization; Lipid peroxidation; Lipids; Liver cancer; Membrane potential; Mitochondria; Nanoparticles; Natural environment; Oxidants; Oxidative stress; Oxidizing agents; p53 Protein; Peroxidation; Reactive oxygen species; Reductases; Research Article; Superoxide dismutase; Surgical implants; Titanium dioxide; Toxicity; Waste Water Technology; Water Management; Water Pollution Control; Oxidative stress; Human health hazard; nanoparticles; Cd pollution; Co-exposure; TiO; Apoptosis
• ISSN: 0944-1344; 1614-7499
• DOI: 10.1007/s11356-019-07130-6

Widespread application of titanium dioxide nanoparticles (nTiO
2
) and ubiquitous cadmium (Cd) pollution may increase their chance of co-existence in the natural environment. Toxicological information on co-exposure of nTiO
2
and Cd in mammalian models is largely lacking. Hence, we studied the combined effects of nTiO
2
and Cd in human liver (HepG2) and breast cancer (MCF-7) cells. We observed that nTiO
2
did not produce toxicity to HepG2 and MCF-7 cells. However, moderate concentration of Cd exposure caused cytotoxicity to both cells. Interestingly, non-cytotoxic concentration of nTiO
2
effectively enhanced the oxidative stress response of Cd indicated by pro-oxidants generation (reactive oxygen species, hydrogen peroxide, and lipid peroxidation) and antioxidants depletion (glutathione level and glutathione reductase, superoxide dismutase, and catalase enzymes). Moreover, nTiO
2
potentiated the Cd-induced apoptosis in both cells suggested by altered expression of p53, bax, and bcl-2 genes along with low mitochondrial membrane potential. Cellular uptake results demonstrated that nTiO
2
facilitates the internalization of Cd into the cells. Overall, this study demonstrated that non-cytotoxic concentration of nTiO
2
enhanced the toxicological potential of Cd in human cells. Therefore, more attention should be paid on the combine effects of nTiO
2
and Cd on human health.