Lei Sheng

TL;DR: The apparent regulation of key ovarian genes supports the hypothesis that TiO(2) NPs directly affects ovarian function, which can accumulate in the ovary and result in ovarian damage, cause an imbalance of mineral element distribution and sex hormones, decrease fertility or the pregnancy rate and oxidative stress in mice.

TL;DR: It is shown that TiO2 NPs can cross the blood-testis barrier to reach the testis and accumulate therein, which, in turn, results in testicular lesions, sperm malformations, and alterations in serum sex hormone levels.

TL;DR: Findings suggest that neuroinflammation may be involved in TiO2 NP-induced alterations of cytokine expression in mouse hippocampus, and more attention should be focused on the application ofTiO2 NPs in the food industry and their long-term exposure effects, especially in the human central nervous system.

TL;DR: TiO2 NPs could be translocated and accumulated in brain, led to oxidative stress, overproliferation of all glial cells, tissue necrosis as well as hippocampal cell apoptosis, and microarray data showed significant alterations in the expression of 249 known function genes, which may be potential biomarkers of brain toxicity caused by TiO1 NPs exposure.

TL;DR: Fertility reduction and ovary injury of mice following exposure to nano-TiO2 may be associated with alteration of inflammation-related or follicular atresia-related cytokine expressions, and humans should take great caution when handling nano- TiO2.