Abstract
Nanosized titanium dioxide (nano-TiO2) has been widely used in consumer products. It can cross the blood-testis barrier (BTB), and it has adverse effects on the male reproductive system. However, the specific mechanism has not been fully elucidated. The purpose of this study was to understand the role of the JNK signaling pathway in the apoptosis and abnormal expression of BTB junction proteins induced by nano-TiO2 in TM4 cells. After different concentration of nano-TiO2 treatments, the cell viability, apoptosis, mitochondrial membrane potential (Δψm), BTB junction proteins (Claudin-11, ZO-1, β-catenin), apoptosis-related proteins (Bax, Bcl-2, cleaved caspase-9, cleaved caspase-3), and phosphorylated (p)-JNK protein were examined. The results showed that cell viability, apoptosis rates, Δψm, and apoptosis-related protein levels changed in a concentration-dependent manner. Cell viability decreased significantly from 100μg/mL nano-TiO2 group. Apoptosis rates increased significantly from 150μg/mL nano-TiO2 group, and Δψm decreased significantly from 150μg/mL nano-TiO2 group. The protein levels of Bax, cleaved caspase-9, and cleaved caspase-3 increased significantly from 150μg/mL nano-TiO2 group, and the protein level of Bcl-2 decreased significantly from 100μg/mL nano-TiO2 group. The protein level of p-JNK increased significantly from 100μg/mL nano-TiO2 group. Abnormal expression of ZO-1 and β-catenin started from 150μg/mL nano-TiO2 group, and abnormal expression of Claudin-11 started from 100μg/mL nano-TiO2 group. Cells were treated with JNK inhibitor SP100625 to determine whether the changes of the above indicators in the concentration of 150μg/mL nano-TiO2 group can be reversed. We found that SP100625 at 20μM significantly reversed these effects. These results highlighted that nano-TiO2 could activate the JNK signaling pathway to induce mitochondria-mediated apoptosis and abnormal expression of BTB junction proteins in TM4 cells.
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