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Methylmercury Induces Alveolar Macrophages Apoptosis

Department of Cosmetic Science, Chia-Nan University of Pharmacy and Science, Tainan, Taiwan

Correspondence: Address correspondence to Tsun-Cheng Kuo, PhD, Department of Cosmetic Science, Chia-Nan University of Pharmacy and Science, 60, Erh-Jen Road, Section 1, Jen-Te, Tainan 717, Taiwan. E-mail:kuotsung{at}mail.chna.edu.tw

Through the use of a scanning electronic microscope, it was found that alveolar macrophages treated with 10 µM of methylmercury for 24 h showed a decrease of surface microvilli, and those treated with 15 µM of methylmercury underwent deformity and subsequent cell death. To investigate their death patterns, DNA was aspirated from alveolar macrophages and analyzed by electrophoresis. It was discovered that the DNA ladder phenomenon became more obvious as the methylmercury increased in concentration. When 5 mM EGTA was used to eliminate calcium ions, a decrease of the ladder phenomenon was observed. Zinc at 1 mM had a similar inhibitory effect. Moreover, an apoptosis peak was observed on flow cytometry analysis of DNA stained with propidium iodide. Alveolar macrophages stained with Hoechst 33342 demonstrated apoptotic bodies induced by methylmercury. The above data indicate that methylmercury can induce a typical apoptosis in alveolar macrophages. Continuing onto the study of the mechanism of apoptosis as induced by methylmercury in alveolar macrophages, it was discovered that methylmercury could increase the intracellular calcium ion concentration and decrease the pH in alveolar macrophages. To find out which endonuclease was responsible for the methylmercury-induced DNA fragmentation of alveolar macrophages, the nuclear proteins of alveolar macrophages was aspirated and tested under different pH values and in conditions with or without calcium ions, and it was discovered that the endonuclease was calcium dependent without relations to pH values.

Key Words: Alveolar Macrophages • Apoptosis • Endonuclease • Methylmercury

International Journal of Toxicology, Vol. 27, No. 3, 257-263 (2008)
DOI: 10.1080/10915810802152095


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