Behaviour of fibrous antigorite on mesothelial Met-5A cell line

This study investigated the cellular toxicity and examined the behaviour of fibrous antigorite on mesothelial Met-5A cell lines, widely employed in studies on the lung diseases, in particular regarding some mechanisms involved in carcinogenesis. Antigorite is a mineral with asbestiform habit found very abundant in serpentinite rocks of the Western Alps, either associated with asbestos chrysotile or tremolite as like the only mineral filling the veins of several rocks. Certain types of fibres originating from natural sources such as asbestos can cause a wide variety of respiratory diseases ranging from inflammation and fibrosis to highly malignant forms of cancers. In this study, the cellular toxicity was determined by measuring antigorite activity on cell viability and membrane integrity by performing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl test (MTT) and measuring lactic dehydrogenase (LDH) release, respectively. The possible induction of oxidative stress from antigorite was examined by both performing a fluorescent analysis of intracellular reactive oxygen species (ROS) production, and evaluating the amount of nitrite/nitrate (NO, nitric oxide) in culture medium. Prostaglandin E2 (PGE2), implicated as having an important role in the pathogenesis of solid tumors through the inhibition of apoptosis, the facilitation of tumor cell invasiveness and the promotion of angiogenesis, by the enzyme-linked immunosorbent assay (ELISA) method was investigated. Fibrous antigorite at 5 μg/ml, 50 μg/ml and 100 μg/ml for 72 h showed dose-dependent cytotoxicity on Met-5A cells. All three doses of antigorite significantly enhanced the ROS production, induced the generation of NO and increased the amount of PGE2. The results of this study revealed significant biochemical changes in mesothelial Met-5A cells after fibrous antigorite treatment and suggested that these changes may directly or indirectly be one of the biological events responsible for eliciting antigorite-mediated host pathological or neoplastic responses.