Modification of DNA structure by reactive nitrogen species as a result of 2-methoxyestradiol-induced neuronal nitric oxide synthase uncoupling in metastatic osteosarcoma cells.

2-methoxyestradiol (2-ME) is a physiological anticancer compound, metabolite of 17β-estradiol. Previously, our group evidenced that from mechanistic point of view one of anticancer mechanisms of action of 2-ME is specific induction and nuclear hijacking of neuronal nitric oxide synthase (nNOS), resulting in local generation of nitro-oxidative stress and finally, cancer cell death. The current study aims to establish the substantial mechanism of generation of reactive nitrogen species by 2-ME.

Neuronal nitric oxide synthase induction in the antitumorigenic and neurotoxic effects of 2-methoxyestradiol.

Objective: 2-Methoxyestradiol, one of the natural 17β-estradiol derivatives, is a novel, potent anticancer agent currently being evaluated in advanced phases of clinical trials. The main goal of the study was to investigate the anticancer activity of 2-methoxy-estradiol towards osteosarcoma cells and its possible neurodegenerative effects. We used an experimental model of neurotoxicity and anticancer activity of the physiological agent, 2-methoxyestradiol.

Methyl-beta-cyclodextrin induces mitochondrial cholesterol depletion and alters the mitochondrial structure and bioenergetics.

There is growing evidence of mitochondrial membrane raft-like microdomains that are involved in the apoptotic pathway. The aim of this study was to investigate the effect of methyl-beta-cyclodextrin (MβCD), being a well-known lipid microdomain disrupting agent and cholesterol chelator, on the structure and bioenergetics of rat liver mitochondria (RLM). We observed that MβCD decreases the function of RLM, induces changes in the mitochondrial configuration state and decreases the calcium chloride-induced swelling.

Coordinate cis-[Cr(C₂O₄)(pm)(OH₂)₂]⁺ Cation as Molecular Biosensor of Pyruvate's Protective Activity Against Hydrogen Peroxide Mediated Cytotoxity.

In this paper instrumental methods of carbon dioxide (CO₂) detection in biological material were compared. Using cis-[Cr(C₂O₄)(pm)(OH₂)₂]⁺ cation as a specific molecular biosensor and the stopped-flow technique the concentrations of CO₂ released from the cell culture medium as one of final products of pyruvate decomposition caused by hydrogen peroxide were determined. To prove the usefulness of our method of CO₂ assessment in the case of biological samples we investigated protective properties of exogenous pyruvate in cultured osteosarcoma 143B cells exposed to 1 mM hydrogen peroxide (H₂O₂) added directly to culture medium.

Pivotal participation of nitrogen dioxide in L-arginine induced acute necrotizing pancreatitis: protective role of superoxide scavenger 4-OH-TEMPO.

For the first time, a direct sensitive method of *NO(2) detection and measurement in biological material has been established. It is based on the interaction of this radical with the coordination compound of Cr(III) with aminodeoxysugar as biosensor. Our new method makes it possible to precisely assess *NO(2) level in experimental acute necrotizing pancreatitis induced by L-arginine, where oxidative and nitrosative stresses are supposed to play a key role in the pathomechanism of the disease.