α-Tocopherol protected against cobalt nanoparticles and cocl₂ induced cytotoxicity and inflammation in Balb/3T3 cells

Abstract

Context: Currently, tissue damage induced by cobalt nanoparticles (CoNPs) and cobalt ions (Co²⁺) are the most serious adverse effect in the patients with metal-on-metal hip prostheses. Therefore, an urgent need exists for the identification of the mechanisms and the development of therapeutic strategies to limit it.

Objective: We aimed to explore the mechanisms of cytotoxicity of CoNPs and Co²⁺ and developed strategies to reduce this cytotoxicity with α-tocopherol treatment.

Methods: To evaluate the protective effect of α-tocopherol, Balb/3T3 cells were pretreated with 10 μM α-tocopherol for 24 h. The cells were then exposed to different concentrations of CoNPs and Co²⁺ for 12 h, 24 h and 48 h. The cell viabilities, reactive oxygen species (ROS), inflammatory cytokines and MAP kinase (MAPK) levels were measured.

Results: CoNPs and Co²⁺ can induce the increase of ROS and inflammatory cytokines in Balb/3T3 cells, such as tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). However, α-tocopherol pretreatment can significantly prevent cytotoxicity induced by CoNPs and Co²⁺, decrease ROS production and decrease levels of inflammatory cytokines in Balb/3T3 cells. Additionally, MAPK pathway may be involved in the protection of α-tocopherol against cytotoxicity induced by CoNPs and Co²⁺ in vitro.

Conclusions: Our results provide new insights into the potential therapeutic use of α-tocopherol in the prevention and treatment of various oxidative- or inflammatory stress-related inflammation and injuries.

Keywords:

• Cobalt
• α-tocopherol
• cytotoxicity
• inflammation
• reactive oxygen species
• MAPK

Disclosure statement

The authors declare that there are no conflicts of interest.