Apoptotic and histopathological defects enhanced by titanium dioxide nanoparticles in male mice after short-term exposure.

Titanium dioxide nanoparticles (TiONPs) are commercially utilized in diverse fields. Therefore, the current study investigated the apoptotic and histopathological defects that were caused in male mice following intraperitoneal (i.p) injection of TiONPs for 28 days. Doses: 2.5, 5.0, 10.0 and 20.0 mg/kg body weight were applied (10 mice for each group). Results revealed that, lactate dehydrogenase (LDH) activity was significantly increased in homogenates of liver, spleen, kidney, lung, heart, and muscles of treated animals, respect to their controls. Also, significant alterations in acid and alkaline phosphatase (ACP and ALP) activities were reported. The dose 5.0 mg/kg exhibited a significant decline in cell viability of blood samples (74.9 %) ( = 0.0177), followed by 2.5 mg/kg (80.8 %), and finally the 10.0 mg/kg (81.8 %) with respect to control (96.3 %). Additionally, significant increases of expressed proteins of caspases-3 and-7 were noticed in cells of the treated animals. Ultrastructural investigations in sections of liver, kidney, lung and spleen of the treated animals showed significant defects, especially in the nucleus, mitochondria and rough endoplasmic reticulum (RER), compared to normal patterns of the control. Also, significant induction of nanoparticle (NPs)-phagolysosomes was visualized in sections of the treated animals. The present findings might provide evidence for the risk pattern of TiONPs in mammals after short-term exposure. So, TiONPs-based commercial products have now increased in the markets, and it is prudent to investigate their mammalian toxicology.