Karlene K. Gunter, Ph.D.

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Studies of the Ca2+ transport system of isolated mitochondria: a) Testing models of mitochondrial divalent cation transport, b) Measuring Ca2+ transport into mitochondria under physiological conditions, in particular with respect to physiological levels and pulses of free cytosolic calcium, c) Measuring properties of newly discovered additional calcium uptake mechanism (RAM) in mitochondria of heart, brain and liver, in particular, effects of pulse height, frequency and the concentration of such cellular components as spermine and Mg2+, and d) Measuring properties of newly discovered calcium rapid efflux mechanism.

Development of pH and membrane potential measurements using fluorescence spectroscopic and microscopic techniques with special attention to their mutual calibration in mitochondria and cells.

Development of free calcium measurements using fluorescence spectroscopic and microscopic techniques with special attention to their mutual calibration in isolated mitochondria and cells. Development of a system to expose isolated mitochondria viewed under a microscope to rapid physiological type pulses of free Ca2+

Studies on the role of mitochondria in calcium transport in the cell: a) Do mitochondria regulate cytosolic calcium levels and if so, under what conditions, b) Are mitochondria involved in hormone response at the cellular level, and if so, what is their role, c) What are the roles of the various mechanisms.

Effects of growth factors on chondrocytes with emphasis on chondrocyte cytosolic [Ca2+] and hypertrophy. How does hypertrophy occur and what is the role of PTHrp?

How is cell metabolism controlled? Can mitochondria respond to physiological pulses of Ca2+ and how is the production of mitochondrial ATP controlled in most cell types?

What is the role of mitochondria in apoptosis? The release of cytochrome c from mitochondria causes apoptosis. What causes this release? Is induction of the permeability transition pore always responsible for the release of cytochrome c or is there another pathway for such release. In particular, can activation of the K uniporter or inhibition of the K/H antiporter cause apoptosis and is this a possible normal mechanism of apoptosis?

Current Appointments

• Research Assistant Professor - Department of Biochemistry and Biophysics (SMD)

Education
PhD Physics	Univ of Cal Berkeley	1968
BS Physics	Mass Inst Technology	1961

Recent Journal Articles
Showing the 5 most recent journal articles. (18 available)
Gunter, T. E.; Gavin, C. E.; Gunter, K. K.;. "The case for manganese interaction with mitochondria". Neurotoxicology 30 (2009): 727-9.
Gunter, T. E.; Gavin, C. E.; Aschner, M.; Gunter, K. K.;. "Speciation of manganese in cells and mitochondria: a search for the proximal cause of manganese neurotoxicity". Neurotoxicology 27 (2006): 765-76.
Gunter KK; Aschner M; Miller LM; Eliseev R; Salter J; Anderson K; Gunter TE. "Determining the oxidation states of manganese in NT2 cells and cultured astrocytes." Neurobiology of aging. 2006; 27(12):1816-26. Epub 2005 Nov 14.
Gunter KK; Aschner M; Miller LM; Eliseev R; Salter J; Anderson K; Hammond S; Gunter TE. "Determining the oxidation states of manganese in PC12 and nerve growth factor-induced PC12 cells." Free radical biology & medicine. 2005; 39(2):164-81. Epub 2005 Mar 31.
Gunter TE; Miller LM; Gavin CE; Eliseev R; Salter J; Buntinas L; Alexandrov A; Hammond S; Gunter KK. "Determination of the oxidation states of manganese in brain, liver, and heart mitochondria." Journal of neurochemistry. 2004; 88(2):266-80.