No abstract

CisPt exerts cytotoxic effects in the neuronal B50 cell line via a caspase-dependent pathway with mitochondria being central relay stations.

No abstract

During apoptosis, apoptosis-inducing factor (AIF) is released from the mitochondrial intermembrane space to the cytosol and to the nucleus. We analyzed AIF in HeLa cells driven to apoptosis by either etoposide or actinomycin D, and we observed changes in the structure and function of mitochondria as well as the translocation of cytochrome c and AIF from mitochondria to the nucleus in early apoptosis. In cells with fragmented chromatin (i.e., in late apoptosis), the immunolabeling for AIF appeared to be distinct from chromatin, being mainly confined to mitochondria.

Cisplatin (cisPt) is a chemotherapy agent used as a treatment for several types of cancer. The main cytotoxic effect of cisplatin is generally accepted to be DNA damage. Recently, the mechanism by which cisPt generates the cascade of events involved in the apoptotic process has been demonstrated. In particular it has been shown that some organelles are cisPt target and are involved in cell death. This paper aims to describe the morphological and functional changes of the Golgi apparatus and lysosomes during apoptosis induced in neuronal rat cells (B50) by cisplatin. The results obtained show that the cellular organelles are the target of cisPt, so their damage can induce cell death.