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Oxidation by thimerosal increases calcium levelsin renal tubular cells.
Chung-Ren Jan1, Bang-Ping Jiann, Yih-Chau Lu
1Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan 813.
Pharmacology & Toxicology
|September 13, 2003
Summary
Thimerosal, a reactive oxidant, increases intracellular calcium levels in kidney cells by releasing calcium from endoplasmic reticulum stores. This process is concentration-dependent and independent of phospholipase C activity.
Area of Science:
- Cell Biology
- Toxicology
- Renal Physiology
Background:
- Cytoplasmic free Ca2+ concentrations ([Ca2+]i) are critical for cellular functions.
- Thimerosal is a reactive oxidant with potential cellular effects.
- Madin Darby canine kidney (MDCK) cells are a model for renal tubular cells.
Purpose of the Study:
- To investigate the effect of thimerosal on [Ca2+]i in MDCK cells.
- To elucidate the mechanism of thimerosal-induced calcium signaling.
Main Methods:
- Measurement of [Ca2+]i using the Ca2+-sensitive dye fura-2.
- Concentration-response analysis to determine EC50.
- Experiments in Ca2+-free medium to assess extracellular Ca2+ dependence.
- Inhibition studies using thapsigargin and U73122.
Main Results:
- Thimerosal induced a concentration-dependent rise in [Ca2+]i with an EC50 of 0.5 microM.
- The calcium signal involved a gradual rise and sustained elevation, with 80% dependent on extracellular Ca2+.
- Thimerosal pretreatment inhibited thapsigargin-induced Ca2+ release in Ca2+-free medium.
- Thimerosal-induced Ca2+ release was independent of phospholipase C activity.
Conclusions:
- Thimerosal triggers intracellular calcium release from endoplasmic reticulum stores in renal tubular cells.
- The mechanism is independent of phospholipase C activation.
- This study clarifies thimerosal's role in calcium homeostasis in kidney cells.