Search

Cyclooxygenase (COX) catalyses the synthesis of prostaglandins from arachidonic acid. There are two isoforms of COX (DuBois et al., 1998; vane et al., 1998). One is constitutively expressed (COX-1) and the other is inducible (COX-2). The COX-2 gene is an immediate, early-response gene that is induced by growth factors, oncogenes, carcinogens, and tumor-promoting phorbol esters (Inoue et al., 1995; Nanayama et al., 1995; Herschman, 1996). The constitutive isoform, COX-1, is essentially unaffected by these factors.

Alteration of many kinds of cellular functions by methylmercury (MM) exposure in vitro have been reported. However, the causal mechanism for the specific dysfunction of nervous systems has not been clarified yet. We have previously demonstrated that microtubules in cultured mouse glioma cells are specifically disrupted by MM before the morphological disorders of the other organelles are detected. This specific impairment of microtubules inhibited cell growth.

Co-administration of selenium compounds with mercuric mercury resulted in remarkable depression of acute toxicity of mercury through 1) reduction of mercury accumulation in the kidneys, a major target of acute toxicity of inorganic mercury, by forming high molecular weight complexes consisting of Hg, Se and proteins in the blood, which were hardly filtered through glomerulus; 2) elongation of retention of mercury and selenium as inert high molecular weight complexes in the blood, especially in the erythrocytes; 3) formation of stable and non-diffusible complexes of Hg and Se in various organs such as the liver and kidneys.

A complex of methylmercury (MeHg) with glutathione (GSH) has been found in several tissues such as brain, liver, erythrocytes and bile. Although the binding of MeHg to GSH is reversible, the complex formation may play an important role in the transport of MeHg.