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Reactive oxygen species are key mediators of the nitric oxide apoptotic pathway in anterior pituitary cells

Leticia I Machiavelli1, Ariel H Poliandri, Fernanda A Quinteros

  • 1Departamento de Química Biológica, IQUIFIB, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.

Nitric Oxide : Biology and Chemistry
|September 26, 2006
PubMed

Insights

Nitric oxide (NO) triggers apoptosis in pituitary cells by increasing reactive oxygen species (ROS). Antioxidants like N-acetyl-cysteine protect cells, highlighting ROS

Area of Science:

  • Cell Biology
  • Biochemistry
  • Endocrinology

Background:

  • Long-term nitric oxide (NO) exposure induces apoptosis in anterior pituitary cells.
  • The precise intracellular signaling pathways mediating NO-induced apoptosis are not fully understood.

Purpose of the Study:

  • To investigate the early molecular mechanisms involved in the nitric oxide (NO) apoptotic cascade in anterior pituitary cells.
  • To elucidate the role of reactive oxygen species (ROS) and antioxidant systems in NO-induced cell death.

Main Methods:

  • Assessment of caspase 3 activation and mitochondrial membrane potential.
  • Measurement of reactive oxygen species (ROS) production.
  • Evaluation of antioxidant enzyme activities (catalase, glutathione peroxidase) and reduced glutathione (GSH) levels.
  • Inhibition studies using N-acetyl-cysteine.

Main Results:

  • Nitric oxide (NO) activated caspase 3 without disrupting mitochondrial membrane potential.
  • NO rapidly increased ROS, dependent on the mitochondrial electron transport chain.
  • N-acetyl-cysteine mitigated ROS increase, caspase 3 activation, and apoptosis.
  • Catalase was inactivated by NO, while glutathione peroxidase (GPx) and reduced glutathione (GSH) levels increased at later time points.

Conclusions:

  • Reactive oxygen species (ROS) are critical triggers of the NO-induced apoptotic cascade in anterior pituitary cells.
  • NO-induced oxidative stress, exacerbated by catalase inhibition, overwhelms cellular antioxidant defenses (GPx, GSH), leading to apoptosis.

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