Sung Min Han

Mechanism of taxol‐induced apoptosis in human SKOV3 ovarian carcinoma cells

Taxol is extensively used clinically for chemotherapy of patients with ovarian, breast, and lung cancer. Although taxol induces apoptosis of cancer cells, its exact mechanism of action is not yet known. To determine the mechanism of action of taxol in ovarian cancer, we tested the effects of the drug, on the human ovarian carcinoma cell line, SKOV3. We observed that taxol‐induced apoptosis of these cells by phosphatidylserine (PS) externalization and DNA fragmentation. While treatment of cells with taxol resulted in bcl‐2 phosphorylation and mitochondrial depolarization, cytochrome c was not released and pro‐caspase‐3 was not activated. Treatment of SKOV3 cells with taxol, however, resulted in the translocation of AIF from the mitochondria to the nucleus via the cytosol. Taken together, these findings suggest that in SKOV3 cells, taxol induces caspase‐independent AIF‐dependent apoptosis.

Changes in magnesium concentration in the serum and cerebrospinal fluid of neuropathic rats

Background:u2002 Central sensitization of neuropathic pain is associated with an influx of extracellular calcium via the opening of N‐methyl‐d‐aspartate (NMDA) receptor‐gated ion channels, which are usually blocked by magnesium plugs. As magnesium‐deficient rats develop a mechanical hyperalgesia and intrathecal or intraperitoneal magnesium suppresses neuropathic pain, the magnesium concentrations in serum and cerebrospinal fluid may be altered in neuropathic pain. We therefore compared the magnesium concentrations in serum and cerebrospinal fluid of neuropathic rats with those in injured rats without symptoms of neuropathic pain and normal rats.