Independent effects of the broccoli-derived compound sulforaphane on Ca²⁺ influx and apoptosis in Madin-Darby canine renal tubular cells

Chin J Physiol. 2010 Aug 31;53(4):215-22. doi: 10.4077/cjp.2010.amk053.


This study explored whether sulforaphane changed basal [Ca²⁺]i levels in suspended Madin-Darby canine kidney (MDCK) cells by using fura-2 as a Ca²⁺-sensitive fluorescent dye. Sulforaphane at concentrations between 2.5-10 microM increased [Ca²⁺]i in a concentration-dependent manner. This Ca²⁺ influx was inhibited by phospholipase A2 inhibitor aristolochic acid but not by Ca²⁺ channel blockers such as nifedipine, nimodipine, nicardipine, diltiazem, verapamil, econazole and SK&F96365. The Ca²⁺ signal was abolished by removing extracellular Ca²⁺. In Ca²⁺-free medium, pretreatment with sulforaphane did not alter the endoplasmic reticulum Ca²⁺ pump inhibitor thapsigargin-induced Ca²⁺ release suggesting sulforaphane did not induce slow Ca²⁺ release from endoplasmic reticulum. At concentrations between 1 and 20 microM, sulforaphane induced concentration-dependent decrease in cell viability which was not affected by pre-chelation of cytosolic Ca²⁺ with BAPTA/AM. Flow cytometry data suggest that 20 (but not 5 and 10) microM sulforaphane induced significant increase in sub G1 phase indicating involvement of apoptosis. Collectively, in MDCK cells, sulforaphane induced [Ca²⁺]i rises by causing Ca²⁺ entry through phospholipase A2-sensitive pathways without inducing Ca²⁺ release from the endoplasmic reticulum. Sulforaphane also induced Ca²⁺-independent cell death that might involve apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Brassica / chemistry*
  • Calcium / metabolism*
  • Cells, Cultured
  • Dogs
  • Isothiocyanates
  • Kidney Tubules / cytology
  • Kidney Tubules / drug effects*
  • Kidney Tubules / metabolism
  • Thiocyanates / pharmacology*


  • Isothiocyanates
  • Thiocyanates
  • sulforafan
  • Calcium