Products of oxidative and non-oxidative metabolism of L-arginine as potential regulators of Ca transport in mitochondria of uterine smooth muscle.

Mitochondria play a crucial role in maintaining Ca homeostasis in cells. Due to the critical regulatory role of the products of oxidative and non-oxidative metabolism of L-arginine, it is essential to clarify their effect on Ca transport in smooth muscle mitochondria. Experiments were performed on the uterine myocytes of rats and isolated mitochondria.

Use of thiacalix[4]arene C-1193 for a directed influence on the functional activity of mitochondria and simulation of this process using a Petri nets.

In molecular biological studies, considerable attention is paid to macrocyclic nanoscale compounds known as calix[4]arenes. An imperative concern in biochemical membranology and molecular biotechnology is the exploration of effectors capable of modifying the intensity of redox reactions within the inner mitochondrial membrane and influencing the activity of its Ca transport systems. The simulation model development is relevant to formalize and generalize the experimental data and assess the conformity of experimental results with theoretical predictions.

Biochemical properties of H-Ca-exchanger in the myometrium mitochondria.

Some biochemical properties of the H-Ca-exchanger in uterine smooth muscle mitochondria have been described. The experiments were performed on a suspension of isolated mitochondria from the myometrium of rats. Methods of confocal microscopy, spectrofluorimetry and photon correlation spectroscopy were used.

NO-synthase activity in mitochondria of uterus smooth muscle: identification and biochemical properties.

Information about the catalytic and kinetic properties of mitochondria NO-synthase from uterus smooth muscle is missing currently. According to the data on MitoTracker Orange CM-H2TMRos and 4-аmino-5-methylamino-2',7'-difluorescein, diaminofluorescein-FM (DAF-FM) dye co-localization in uterine smooth muscle cells, presented in this paper, NO can be synthesized in their mitochondria. High activity of NO synthase requires the presence of substrates of respiration, L-arginine, Ca2+ and NADPH.