Mammalian skeletal and cardiac muscle cells carry type-1 porin, the gene product of VDAC1, in mitochondrial outer membranes, cell membranes and even other cell compartments (Junankar PR et al., 1995, J Muscle Res Cell Motil 16, 595ff).

The application of monoclonal anti-type-1 porin/VDAC antibodies or DIDS, respectively, blocked the regulatory volume decrease (RVD) of HeLa cells exposed to hypotonic stimulation (Thinnes FP et al., 2000, Molec Gen Metab 69, 331ff). Corresponding reactions were seen in epithelial cells of VDAC1 knock out mice (Okada, SF et al., 2004, J Gen Physiol 124, 513ff). In accord, it has been shown that anti-type-1 porin/VDAC antibodies abolish the apoptotic volume decrease (AVD) of stimulated cells (Elinder F et al., 2005, Cell Death Differ 12, 1134ff).

The formula: “ACC ∼ Icl swell ∼ ICOR ∼ ORCC ∼ ORDIC ∼ VRAC ∼ VRCC ∼ VSOAC = cell membrane standing VDAC modulated by varying regulators” represents a synoptic interpretation of these data (Thinnes FP, 2009, Mol Gen Metab 97, 92ff; Thinnes FP, 2010, AJP in press).

Concerning the context here, it was recently evidenced by use of different approaches that 1) type-1 porin/VDAC is localized at the plasma membrane of septal and hippocampal neurons, 2) the channel here is concentrated in caveolae, and 3) it is associated with the membranal estrogen receptor (ERα) and also with caveolin-1 (Marin R, 2007, Mol Membr Biol 24, 148ff). The group has, meanwhile, confirmed their data and also its relevance for Alzheimer´s disease research (Ramirez CM et al., 2009, Mol Cell Neurosci 42, 172ff).

However, considering these data might help to better understand the results concerning tamoxifen and DIDS effects as presented here by Kozera and colleges.