Bupivacaine myotoxicity is mediated by mitochondria

TL;DR: It is shown that Col6a1−/− muscles have a loss of contractile strength associated with ultrastructural alterations of sarcoplasmic reticulum and mitochondria and spontaneous apoptosis, which indicates that collagen VI myopathies have an unexpected mitochondrial pathogenesis that could be exploited for therapeutic intervention.

TL;DR: Compared with bupivacaine, which induces both necrosis and apoptosis, the tissue damage caused by ropvacaine is significantly less severe, and it is concluded that ropavacaine’s myotoxic potential is more moderate in comparison with that of bup Vivacaine.

TL;DR: Evidence supporting the existence of distinct functional phenotypes in mitochondria from slow and fast fibers that may be required to ensure optimal muscle function is reviewed.

TL;DR: Results show dose- and time-dependent cytotoxic effects of lidocaine on bovine articular chondrocytes, and suggest that local anesthetics as a class of drugs may negatively affect articular cartilage.

TL;DR: Using an improved method of gel electrophoresis, many hitherto unknown proteins have been found in bacteriophage T4 and some of these have been identified with specific gene products as mentioned in this paper.

TL;DR: The identification and cloning of an apoptosis-inducing factor, AIF, which is sufficient to induce apoptosis of isolated nuclei is reported, indicating that AIF is a mitochondrial effector of apoptotic cell death.

TL;DR: Current evidence that the pore complex is involved in outer-membrane rupture and release of these proteins during programmed cell death is reviewed, along with indications that transient pore opening may provoke 'accidental' apoptosis.

TL;DR: The identification and characterization of another nuclease that is specifically activated by apoptotic stimuli and is able to induce nucleosomal fragmentation of DNA in fibroblast cells from embryonic mice lacking DFF is reported.