CommentaryRuthenium red as a tool to study calcium channels, neuronal death and the function of neural pathways
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2022, PhytomedicineCitation Excerpt :To determine the source of Ca2+, we pretreated cells with ruthenium red (RR) (200 nM, 30 min), thapsigargin (300 nM, 30 min), and glycyl-L-phenylalanine 2-naphthylamine (GPN) (200 µM, 30 min). RR is a non-competitive inhibitor of the mitochondrial Ca2+ uniporter, which could inhibit mitochondrial Ca2+ uptake in cells (TAPIA and VELASCO, 1997). Thapsigargin can deplete endoplasmic reticulum (ER) Ca2+ stores by blocking ER Ca2+-ATPase (Uchida et al., 2021).
Zn<sup>2+</sup> entry through the mitochondrial calcium uniporter is a critical contributor to mitochondrial dysfunction and neurodegeneration
2020, Experimental NeurologyCitation Excerpt :Interestingly, a critical target of acute deleterious Zn2+ effects also appears to be the mitochondria—which Zn2+ also enters through the MCU—to potently trigger mitochondrial dysfunction (Clausen et al., 2013; Gazaryan et al., 2007; Ji et al., 2019; Jiang et al., 2001; Malaiyandi et al., 2005; Saris and Niva, 1994). However, past studies elucidating the role of the MCU in Zn2+ effects were limited to the use of pharmacologic MCU blockers which lack complete specificity (Tapia and Velasco, 1997). Consequently, one cannot be certain that beneficial effects are specifically due to MCU blockade.
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