Collectively, our data indicate that the mitochondria-dependent apoptotic pathway is one of the major routes operating in osteoclasts. In the current study, we measured SI, -cell function, and plasma levels of IL-6 and TNF- after treatment of chromium chloride (GaCr) in T2D. This might be due to the ability of decreasing interleukin-6 (IL-6) and tumor necrosis factor (TNF-) shown in animal studies. Cytosolic cytochrome c participated in activating caspase-3 and -9, both required for apoptosis. Trivalent chromium has shown to improve SI in our previous study. Protein levels of Bcl-2 and Bc-xL were decreased before apoptosis, whereas expression of wild-type Bcl-2 repressed apoptosis, confirming that cytochrome c release is critical in initiating apoptosis. Cytosolic cytochrome c was originated from a single mitochondrial compartment, supporting a common pool involved in respiration and apoptosis, and it was chemically identical to the native form, with no indication of oxidative or nitrative modifications. Trapping H(2)O(2)-derived hydroxyl radical decreased apoptosis. With the addition of a mitochondrial uncoupler, H(2)O(2) production and apoptosis were blocked, indicating the prominent role of mitochondria-derived H(2)O(2). There are only three studies in humans with controversial results. H(2)O(2) production was increased during culture, preceding cytochrome c release both processes occurred anterior to apoptosis. The findings of this review indicate, based on in vitro and in vivo studies, that chromium might have potential anti-inflammatory properties, but some of the studies did not show anti-inflammatory effects for chromium (two studies). These questions were investigated using osteoclasts, because they are rich in mitochondria and because osteoclast apoptosis is critical in bone metabolism regulation. Two unresolved aspects of the role of mitochondria-derived cytochrome c in apoptosis are whether there is a separate pool of cytochrome c within mitochondria that participates in the activation of apoptosis and whether a chemically modified cytochrome c drives apoptosis.
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