[Plaferon lb as a protector of radioinducible disorder].
As it is known, p-53-dependent apoptosis is the cause of the radiosensitive cells' rapid death during the first ours after gamma-irradiation. It is considered, that short time suppression of the function of p-53 may decrease injury of normal tissue. The aim of our study was the determination of the effectiveness and possible mechanisms of radioprotective features of plaferon LB. It was found that plaferon LB provides correction of content and function of nitric oxide in hepatocytes during gamma-irradiation and that may be induced by its antioxidant capabilities. By the correction of oxidative metabolism plaferon LB decreases intensity of postradiation alterations. The restriction of intensification of nitric oxide synthesis after irradiation also results in decreasing of iNOS expression. Plaferon LB induces reduction of oxidative stress in the organism, also provides NO-modulatory activity. Increase of proapoptotic activity of p-53 is due to NO-stimulated DNA-dependent protein kinase and p-38 mitogen activated protein kinase. It may be concluded that during gamma-irradiation the preliminary influence of plaferon LB provides prevention of hyperproduction of nitric oxide and by this way promotes suppression of NO-inducible activation of p-53-induced apoptosis.
Saralidze
M A
MA
Datunashvili
I V
IV
Machavariani
M G
MG
Enukidze
M G
MG
Pavliashvili
A T
AT
D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D022781:Hepatocytes / Q000378:metabolism; D009479:Neuropeptides / Q000627:therapeutic use*; D009569:Nitric Oxide / Q000378:metabolism; D011833:Radiation Injuries, Experimental / Q000378:metabolism / Q000517:prevention & control*; D051381:Rats
D000975:Antioxidants; D009479:Neuropeptides; C091912:plaferon; D009569:Nitric Oxide