Apoptosis induced by Na+/H+ antiport inhibition activates the LEI/L-DNase II pathway.

L-DNase II is derived from its precursor leucocyte elastase inhibitor (LEI) by post-translational modification. In vitro, the conversion of LEI into L-DNase II can be induced by incubation of LEI at an acidic pH. In this study, we proposed to analyze the effects of intracellular acidification on this transformation.

Elastase is not required for L-DNase II activation during apoptosis in developing chicken neural retina.

During retinal development, the neuronal death is carried out by the mechanism of apoptosis. Among the different endonucleases activated, L-DNase II seems to be responsible for most of DNA degradation in this tissue. L-DNase II derives from LEI (Leukocyte Elastase Inhibitor) by a post-translational modification carried out by elastase in apoptosis induced in vitro.

A caspase-independent cell clearance program. The LEI/L-DNase II pathway.

The discovery of caspase-mitochondrial pathway counts as one of the most important discovery in apoptosis biochemistry. Today, however, we begin to recognize its limits. Inhibition of caspase does not prevent cell death in many mammalian models.

Major strain differences in response to chronic systemic administration of the mitochondrial toxin 3-nitropropionic acid in rats: implications for neuroprotection studies.

Chronic systemic treatment with 3-nitropropionic acid in rats produces persistent dystonia and bradykinesia, and striatal lesions reminiscent of Huntington's disease. However, the interpretation of results obtained with this model are complicated by a heterogeneous distribution of the response to a given toxic dose of 3-nitropropionic acid: approximately half of the animals develop selective striatal lesions, which in certain cases are associated with extrastriatal lesions, and the other half are apparently spared. Thus, the chronic 3-nitropropionic acid lesion model can be difficult for neuroprotection studies in which a consistent response to neurotoxic treatment is prerequisite.