Toxic effect and mechanism of ultrafine carbon black on mouse primary splenocytes and two digestive enzymes.

This paper investigated the toxic effect and mechanism of ultrafine carbon black (UFCB) on splenocytes and enzymes in the digestive system. It was found that the toxicity of UFCB to splenocytes was dose-dependent. UFCB with a low concentration (< 15 μg/mL) had no significant effect on splenocytes while UFCB with high concentration (> 15 μg/mL) induced significant oxidative damage with increased content of reactive oxygen species (ROS) (134%) and malonaldehyde (MDA) (222.3%) along with the decreased activity of superoxide dismutase (SOD) (55.63%) and catalase (CAT) (87.73%). Analysis combined cellular and molecular levels indicated that UFCB induced splenocyte toxicity through oxidative stress. The interactions of UFCB with two important digestive enzymes, α-amylase and lipase, were also studied respectively. Results showed that the interaction of UFCB and the two enzymes altered the particle size and fluorescence intensity in both experimental systems. The formation of protein corona also resulted in the contraction of the polypeptide skeleton in both enzymes, which further inhibited their activity. Our work provided basic data on the toxicity of UFCB in the spleen and digestive system and fills the gap in the study of UFPs toxicity. UFCB induced splenocyte toxicity and enzyme dysfunction through oxidative stress and protein corona formation respectively. ga1 • UFCB has toxicity on splenocytes through oxidative stress. • The binding mechanism of UFCB with α-amylase and lipase were investigated. • UFCB changed the structure and function of α-amylase and lipase. • The toxicity of UFCB to lipase is greater than that of α-amylase. • A combined molecular and cellular toxicity evaluation method was established. [ABSTRACT FROM AUTHOR]