30 research outputs found
Impact of a tobacco smoke on a metabolism of an organ culture of bovine lenses and potential protection by antioxidants
Smoke from cigarette smoking (CS) has been proposed to be a major
environmental risk factor for a variety of human diseases and was implicated also in
cataract, an eye lens pacification, which is a major cause of blindness. We have undertaken
a study to investigate the effect of smoke on the physiological integrity and metabolism of
organ cultured lenses. Lenses in organ culture
are metabolically active and have functional
defense systems, thus they pr
ovide an appropriate model for studying the effects of smoke.
Also possible protective action of N-acetyl
L-cysteine (NAC) which is a precursor of
glutathione and the iron chelator Deferoxamine (DFO), was estimated as potential protective
agents against cataract.ΠΡΠ΅Π΄ΠΏΠΎΠ»Π°Π³Π°Π΅ΡΡΡ, ΡΡΠΎ
Π΄ΡΠΌ ΠΎΡ ΠΊΡΡΠ΅Π½ΠΈΡ ΡΠΈΠ³Π°ΡΠ΅Ρ (ΠΠ‘)
ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΎΡΠ½ΠΎΠ²Π½ΡΠΌ ΡΠΊΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΌ ΡΠ°ΠΊΡΠΎΡΠΎΠΌ ΡΠΈΡΠΊΠ° Π΄Π»Ρ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΌΠ½ΠΎΠΆΠ΅ΡΡΠ²Π°
Π±ΠΎΠ»Π΅Π·Π½Π΅ΠΉ ΡΠ΅Π»ΠΎΠ²Π΅ΠΊΠ° ΠΈ ΠΌΠΎΠΆΠ΅Ρ ΡΠ°ΠΊΠΆΠ΅ Π²ΡΠ·Π²Π°ΡΡ ΡΠ°Π·Π²ΠΈΡΠΈΠ΅ ΠΊΠ°ΡΠ°ΡΠ°ΠΊΡΡ, ΠΏΠΎΠΌΡΡΠ½Π΅Π½ΠΈΡ
Ρ
ΡΡΡΡΠ°Π»ΠΈΠΊΠ° Π³Π»Π°Π·Π°, ΡΡΠΎ ΡΠ²Π»ΡΠ΅ΡΡΡ Π³Π»Π°Π²Π½ΠΎΠΉ
ΠΏΡΠΈΡΠΈΠ½ΠΎΠΉ ΡΠ»Π΅ΠΏΠΎΡΡ. ΠΡΠ»ΠΎ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΎ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ Π΄Π»Ρ ΠΈΠ·ΡΡΠ΅Π½ΠΈΡ Π²ΠΎΠ·Π΄Π΅ΠΉΡΡΠ²ΠΈΡ
Π΄ΡΠΌΠ° Π½Π° ΡΠΈΠ·ΠΈΠΎΠ»ΠΎΠ³ΠΈΡ
Π΅ΡΠΊΡΡ ΡΠ΅Π»ΠΎΡΡΠ½ΠΎΡΡΡ
ΠΈ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌ ΠΎΡΠ³Π°Π½Π½ΠΎΠΉ ΠΊΡΠ»ΡΡΡΡΡ Ρ
ΡΡΡΡΠ°Π»ΠΈΠΊΠΎΠ² Π³Π»Π°Π·Π°. Π₯ΡΡΡΡΠ°Π»ΠΈΠΊΠΈ Π³Π»Π°Π·Π° Π² ΠΎΡΠ³Π°Π½Π½ΠΎΠΉ
ΠΊΡΠ»ΡΡΡΡΠ΅ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΡΠ΅ΡΠΊΠΈ Π°ΠΊΡΠΈΠ²Π½Ρ ΠΈ ΠΈΠΌΠ΅ΡΡ ΡΡΠ½ΠΊΡΠΈΠΎΠ½Π°Π»ΡΠ½ΡΠ΅ ΡΠΈΡΡΠ΅ΠΌΡ Π·Π°ΡΠΈΡΡ,
ΡΠ°ΠΊΠΈΠΌ ΠΎΠ±ΡΠ°Π·ΠΎΠΌ ΠΎΠ½ΠΈ ΡΠ²Π»ΡΡΡΡΡ ΠΎΠΏΡΠΈΠΌΠ°Π»ΡΠ½ΠΎΠΉ ΠΌΠΎΠ΄Π΅Π»ΡΡ Π΄Π»Ρ ΠΈΠ·ΡΡΠ΅Π½ΠΈΡ Π²ΠΎΠ·Π΄Π΅ΠΉΡΡΠ²ΠΈΡ
Π΄ΡΠΌΠ°. Π’Π°ΠΊΠΆΠ΅ Π±ΡΠ»ΠΎ ΠΎΡΠ΅Π½Π΅Π½ΠΎ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΠ΅
Π·Π°ΡΠΈΡΠ½ΠΎΠ΅ Π΄Π΅ΠΉΡΡΠ²ΠΈΠ΅ N-Π°ΡΠ΅ΡΠΈΠ» L-ΡΠΈΡΡΠ΅ΠΈΠ½Π° (NAC), ΠΊΠΎΡΠΎΡΡΠΉ ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΈΡΡ
ΠΎΠ΄Π½ΡΠΌ
Π²Π΅ΡΠ΅ΡΡΠ²ΠΎΠΌ Π΄Π»Ρ Π³Π»ΡΡΠ°ΡΠΈΠΎΠ½Π° ΠΈ Ρ
Π΅Π»Π°ΡΠΈΡΡΡΡΠ΅Π³ΠΎ Π°Π³Π΅Π½ΡΠ° ΠΆΠ΅Π»Π΅Π·Π° Π΄Π΅ΡΠ΅ΡΠΎΠΊΡΠ°ΠΌΠΈΠ½Π°
(DFO) ΠΊΠ°ΠΊ ΠΏΠΎΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½ΡΡ
Π·Π°ΡΠΈΡΠ½ΡΡ
Π²Π΅ΡΠ΅ΡΡΠ² ΠΏΡΠΎΡΠΈΠ² ΠΊΠ°ΡΠ°ΡΠ°ΠΊΡΡ.ΠΠ΅ΡΠ΅Π΄Π±Π°ΡΠ°ΡΡΡΡΡ, ΡΠΎ Π΄ΠΈΠΌ Π²ΡΠ΄ ΠΏΠ°Π»ΡΠ½Π½Ρ ΡΠΈΠ³Π°ΡΠ΅Ρ (ΠΠ‘)
Ρ ΠΎΡΠ½ΠΎΠ²Π½ΠΈΠΌ Π΅ΠΊΠΎΠ»ΠΎΠ³ΡΡΠ½ΠΈΠΌ ΡΠ°ΠΊΡΠΎΡΠΎΠΌ ΡΠΈΠ·ΠΈΠΊΡ Π΄Π»Ρ ΡΠΎΠ·Π²ΠΈΠ½Π΅Π½Π½Ρ Π±Π°Π³Π°ΡΡΠΎΡ
Ρ
Π²ΠΎΡΠΎΠ± Π»ΡΠ΄ΠΈΠ½ΠΈ Ρ ΠΌΠΎΠΆΠ΅ ΡΠ°ΠΊΠΎΠΆ Π²ΠΈΠΊΠ»ΠΈΠΊΠ°ΡΠΈ ΡΠΎΠ·Π²ΠΈΠ½Π΅Π½Π½Ρ ΠΊΠ°ΡΠ°ΡΠ°ΠΊΡΠΈ, ΠΏΠΎΠΌΡΡΠ½ΡΠ½Π½Ρ ΠΊΡΠΈΡΡΠ°Π»ΠΈΠΊΠ°
ΠΎΠΊΠ°, ΡΠΎ Ρ Π³ΠΎΠ»ΠΎΠ²Π½ΠΎΡ ΠΏΡΠΈΡΠΈΠ½ΠΎΡ ΡΠ»ΡΠΏΠΎΡΠΈ.
ΠΡΠ»ΠΎ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΎ Π΄ΠΎΡΠ»ΡΠ΄ΠΆΠ΅Π½Π½Ρ Π΄Π»Ρ Π²ΠΈΠ²ΡΠ΅Π½Π½Ρ Π²ΠΏΠ»ΠΈΠ²Ρ Π΄ΠΈΠΌΡ Π½Π° ΡΡΠ·ΡΠΎΠ»ΠΎΠ³ΡΡΠ½Ρ ΡΡΠ»ΡΡΠ½ΡΡΡΡ
Ρ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΡΠ·ΠΌ ΠΎΡΠ³Π°Π½Π½ΠΎΡ
ΠΊΡΠ»ΡΡΡΡΠΈ ΠΊΡΠΈΡΡΠ°Π»ΠΈΠΊΡΠ² ΠΎΠΊΠ°. ΠΡΠΈΡΡΠ°Π»ΠΈΠΊΠΈ ΠΎΠΊΠ°
Π²
ΠΎΡΠ³Π°Π½Π½ΡΠΉ ΠΊΡΠ»ΡΡΡΡΡ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΡΡΠ½ΠΎ Π°ΠΊΡΠΈΠ²Π½Ρ ΡΠ°
ΠΌΠ°ΡΡΡ ΡΡΠ½ΠΊΡΡΠΎΠ½Π°Π»ΡΠ½Ρ ΡΠΈΡΡΠ΅ΠΌΠΈ Π·Π°Ρ
ΠΈΡΡΡ,
ΡΠ°ΠΊΠΈΠΌ ΡΠΈΠ½ΠΎΠΌ Π²ΠΎΠ½ΠΈ Ρ ΠΎΠΏΡΠΈΠΌΠ°Π»ΡΠ½ΠΎΡ ΠΌΠΎΠ΄Π΅Π»Π»Ρ Π΄Π»Ρ Π²ΠΈΠ²ΡΠ΅Π½Π½Ρ Π²ΠΏΠ»ΠΈΠ²Ρ Π΄ΠΈΠΌΡ. Π’Π°ΠΊΠΎΠΆ Π±ΡΠ»Π°
ΠΎΡΡΠ½Π΅Π½Π° ΠΌΠΎΠΆΠ»ΠΈΠ²Π° Π·Π°Ρ
ΠΈΡΠ½Π° Π΄ΡΡ N β Π°ΡΠ΅ΡΠΈΠ» β L- ΡΠΈΡΡΠ΅ΡΠ½Π° (NAC), ΠΊΠΎΡΡΠΈΠΉ Ρ Π²ΠΈΡ
ΡΠ΄Π½ΠΎΡ ΡΠ΅ΡΠΎΠ²ΠΈΠ½ΠΎΡ Π΄Π»Ρ Π³Π»ΡΡΠ°ΡΡΠΎΠ½Π° ΡΠ° Ρ
Π΅Π»Π°ΡΠΈΡΡΡΡΠΎΠ³ΠΎ Π°Π³Π΅Π½ΡΠ° Π·Π°Π»ΡΠ·Π° Π΄Π΅ΡΠ΅ΡΠΎΠΊΡΠ°ΠΌΡΠ½Π°
(DFO) ΡΠΊ ΠΏΠΎΡΠ΅Π½ΡΡΠΉΠ½ΠΈΡ
Π·Π°Ρ
ΠΈΡΠ½ΠΈΡ
ΡΠ΅ΡΠΎΠ²ΠΈΠ½
ΠΏΡΠΎΡΠΈ ΠΊΠ°ΡΠ°ΡΠ°ΠΊΡΠΈ
The effects of antioxidants on diabetic damage with a tobacco smoke in bovine lenses
Investigated the mechanisms involved in the effects of preventing cataract and
cigarette smoking (CS) when exposed to the lens antioxidants. Bovine lenses were
removed in organ culture for 12 days, exposed to glucose 450 mg % for antioxidants
including-Desferioxamine (DFO) and cysteine N-acetyl-L-(NAC). Treated lenses were 4
days in culture medium saturated with cigarette smoke daily dose at 500 psi. The use
of laser-lens optical quality was assessed daily. At the end of the incubation period,
lenses were analyzed using an inverted microscopy as epithelial layer was used for
histochemical assessment method Einarson nucleic acids -RNA-DNA staining.
Reactive Oxygen Species (ROS) were evaluated C6827, to measure the level of
cellular oxidation in the epithelial cells of the lens relative to the control cultures by
fluorescence microscopy. High glucose with a smoke causes optical and morphological changes in epithelial cells (hypertrophy, hyperplasia). Antioxidants reduce the
damage caused by high glucose and CS, to protect the lens from high glucose,
reduce cell damage, prevent the increased activity of ROS. NAC protected the lens
from damage high glucose better than DFO. We suggest that NAC can serve as an
effective advocate for the lens of the eye against damage from smoking diabetics.ΠΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π»ΠΈΡΡ ΠΌΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌΡ Π΄Π΅ΠΉΡΡΠ²ΠΈΡ Π°Π½ΡΠΈΠΎΠΊΡΠΈΠ΄Π°Π½ΡΠΎΠ² Π½Π° ΠΏΡΠ΅Π΄ΠΎΡΠ²ΡΠ°ΡΠ΅Π½ΠΈΠ΅ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΊΠ°ΡΠ°ΡΠ°ΠΊΡΡ Ρ ΠΊΡΡΡΡΠΈΡ
.
ΠΡΡΡΠΈ Ρ
ΡΡΡΡΠ°Π»ΠΈΠΊΠΈ Π±ΡΠ»ΠΈ Π²ΡΠ΄Π΅ΡΠΆΠ°Π½Ρ Π²
ΠΊΡΠ»ΡΡΡΡΠ°Π»ΡΠ½ΠΎΠΉ ΡΡΠ΅Π΄Π΅, ΡΠΎΠ΄Π΅ΡΠΆΠ°ΡΠ΅ΠΉ 450
ΠΌΠ³ Π³Π»ΡΠΊΠΎΠ·Ρ Π½Π° 100 Π³ ΡΠ°ΡΡΠ²ΠΎΡΠ° ΠΈ Ρ Π°Π½ΡΠΈΠΎΠΊΠΈΡΠ»ΠΈΡΠ΅Π»ΡΠΌΠΈ β Π΄Π΅ΡΡΠ΅ΡΠΎΠΊΡΠ°ΠΌΠΈΠ½ΠΎΠΌ
(DFO) ΠΈ N-Π°ΡΠ΅ΡΠΈΠ»-L-ΡΠΈΡΡΠ΅ΠΈΠ½ΠΎΠΌ (NAC) Π²
ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ 12 Π΄Π½Π΅ΠΉ. Π’Π°ΠΊ ΠΆΠ΅ 4 Π΄Π½Ρ Ρ
ΡΡΡΡΠ°Π»ΠΈΠΊΠΈ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π»ΠΈΡΡ Π² ΠΊΡΠ»ΡΡΡΡΠ°Π»ΡΠ½ΠΎΠΉ ΡΡΠ΅Π΄Π΅, Π½Π°ΡΡΡΠ°Π΅ΠΌΠΎΠΉ ΠΏΠ°ΠΏΠΈΡΠΎΡΠ½ΡΠΌ Π΄ΡΠΌΠΎΠΌ,
Π΅ΠΆΠ΅Π΄Π½Π΅Π²Π½Π°Ρ Π΄ΠΎΠ·Π° ΠΊΠΎΡΠΎΡΠΎΠ³ΠΎ ΡΠΎΡΡΠ°Π²Π»ΡΠ»Π°
500 psi. ΠΠΏΡΠΈΡΠ΅ΡΠΊΠΎΠ΅ ΠΊΠ°ΡΠ΅ΡΡΠ²ΠΎ Ρ
ΡΡΡΡΠ°Π»ΠΈΠΊΠΎΠ² Π΅ΠΆΠ΅Π΄Π½Π΅Π²Π½ΠΎ ΠΎΡΠ΅Π½ΠΈΠ²Π°Π»ΠΎΡΡ Ρ ΠΏΠΎΠΌΠΎΡΡΡ
Π»Π°Π·Π΅ΡΠ½ΠΎΠΉ ΡΡΡΠ°Π½ΠΎΠ²ΠΊΠΈ. Π ΠΊΠΎΠ½ΡΠ΅ ΠΈΠ½ΠΊΡΠ±Π°ΡΠΈΠΎΠ½Π½ΠΎΠ³ΠΎ ΠΏΠ΅ΡΠΈΠΎΠ΄Π° Ρ
ΡΡΡΡΠ°Π»ΠΈΠΊΠΈ Π±ΡΠ»ΠΈ
ΠΈΠ·ΡΡΠ΅Π½Ρ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΈΠ½Π²Π΅ΡΡΠΈΠΎΠ½Π½ΠΎΠΉ ΠΌΠΈΠΊΡΠΎΡΠΊΠΎΠΏΠΈΠΈ, a ΡΠΏΠΈΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΡΠΉ ΡΠ»ΠΎΠΉ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π»ΡΡ Π΄Π»Ρ Π³ΠΈΡΡΠΎΡ
ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΌΠ΅ΡΠΎΠ΄Π°
ΠΎΡΠ΅Π½ΠΊΠΈ Π½ΡΠΊΠ»Π΅ΠΈΠ½ΠΎΠ²Ρx ΠΊΠΈΡΠ»ΠΎΡ ΠΎΠΊΡΠ°ΡΠΈΠ²Π°Π½ΠΈΠ΅ΠΌ ΠΠΠ-Π ΠΠ ΠΏo ΠΌΠ΅ΡΠΎΠ΄Ρ ΠΠΉΠ½Π°ΡΡΠΎΠ½Π°.
ΠΠΊΡΠΈΠ²Π½ΡΠ΅ ΡΠΎΡΠΌΡ ΠΊΠΈΡΠ»ΠΎΡΠΎΠ΄Π° (ROS) Π±ΡΠ»ΠΈ
ΠΎΡΠ΅Π½Π΅Π½Ρ Π² ΡΠΏΠΈΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΊΠ°Ρ
Ρ
ΡΡΡΡΠ°Π»ΠΈΠΊΠ° Ρ ΠΏΠΎΠΌΠΎΡΡΡ ΡΠ»yΠΎΡΠ΅ΡΡΠ΅Π½ΡΠ½ΠΎΠΉ
ΠΌΠΈΠΊΡΠΎΡΠΊΠΎΠΏΠΈΠΈ Π΄Π»Ρ ΠΈΠ·ΠΌΠ΅ΡΠ΅Π½ΠΈΡ ΡΡΠΎΠ²Π½Ρ
ΠΊΠ»Π΅ΡΠΎΡΠ½ΠΎΠ³ΠΎ ΠΎΠΊΠΈΡΠ»Π΅Π½ΠΈΡ ΠΎΡΠ½ΠΎΡΠΈΡΠ΅Π»ΡΠ½ΠΎ
ΠΊΠΎΠ½ΡΡΠΎΠ»ΡΠ½ΡΡ
ΠΊΡΠ»ΡΡΡΡ. ΠΡΡΠΎΠΊΠ°Ρ Π΄ΠΎΠ·Π° Π³Π»ΡΠΊΠΎΠ·Ρ Ρ Π΄ΡΠΌΠΎΠΌ Π²ΡΠ·ΡΠ²Π°Π΅Ρ ΠΎΠΏΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈ
ΠΌΠΎΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ Π² ΡΠΏΠΈΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΊΠ°Ρ
(Π³ΠΈΠΏΠ΅ΡΡΡΠΎΡΠΈΡ, Π³ΠΈΠΏΠ΅ΡΠΏΠ»Π°Π·ΠΈΡ) ΠΈ ΡΠ²Π΅Π»ΠΈΡΠΈΠ²Π°Π΅Ρ ΡΠ»yΠΎΡΠ΅ΡΡΠ΅Π½ΡΠΈΡ.
ΠΠ½ΡΠΈΠΎΠΊΡΠΈΠ΄Π°Π½ΡΡ ΡΠΌΠ΅Π½ΡΡΠ°ΡΡ ΡΡΠΎ Π²ΠΎΠ·Π΄Π΅ΠΉΡΡΠ²ΠΈΠ΅, ΡΠ½ΠΈΠΆΠ°ΡΡ ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²ΠΎ ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½Π½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ, ΠΏΡΠ΅Π΄ΠΎΡΠ²ΡΠ°ΡΠ°ΡΡ ΡΠ²Π΅Π»ΠΈΡΠ΅Π½Π½ΡΡ Π΄Π΅ΡΡΠ΅Π»ΡΠ½ΠΎΡΡΡ ROS. NAC Π·Π°ΡΠΈΡΠΈΠ»
Π»ΠΈΠ½Π·Ρ ΠΎΡ ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΡ Π½Π΅ΡΠΊΠΎΠ»ΡΠΊΠΎ Π»ΡΡΡΠ΅, ΡΠ΅ΠΌ DFO. ΠΡ ΠΏΡΠ΅Π΄ΠΏΠΎΠ»Π°Π³Π°Π΅ΠΌ, ΡΡΠΎ
Π΄Π°Π½Π½ΡΠ΅ Π°Π½ΡΠΈΠΎΠΊΠΈΡΠ»ΠΈΡΠ΅Π»ΠΈ ΠΌΠΎΠ³ΡΡ ΡΠ»ΡΠΆΠΈΡΡ
ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΡΠΌ ΡΡΠ΅Π΄ΡΡΠ²ΠΎΠΌ Π·Π°ΡΠΈΡΡ Ρ
ΡΡΡΡΠ°Π»ΠΈΠΊΠ° Π³Π»Π°Π·Π° ΠΏΡΠΎΡΠΈΠ² ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΡ Ρ
ΠΊΡΡΡΡΠΈΡ
Π΄ΠΈΠ°Π±Π΅ΡΠΈΠΊΠΎΠ². Π’Π°ΠΊΠΈΠΌ ΠΎΠ±ΡΠ°Π·ΠΎΠΌ,
ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ Π°Π½ΡΠΈΠΎΠΊΠΈΡΠ»ΠΈΡΠ΅Π»ΡΠ½ΡΡ
Π²Π΅ΡΠ΅ΡΡΠ²
Π² ΠΏΡΠΎΡΠΈΠ»Π°ΠΊΡΠΈΠΊΠ΅ ΠΊΠ°ΡΠ°ΡΠ°ΠΊΡΡ y
ΠΊΡΡΠΈΠ»ΡΡΠΈΠΊoΠ² ΠΈ Π»Π΅ΡΠ΅Π½ΠΈΠ΅ β ΠΎΡΠ΅Π½Ρ ΠΏΡΠΈΠ²Π»Π΅ΠΊΠ°ΡΠ΅Π»ΡΠ½Π°Ρ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΡΡΡ, ΠΊΠΎΡΠΎΡΠ°Ρ
ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Π½ΠΎΠΉ Π±ΠΎΠ»Π΅Π΅ Π³Π»ΡΠ±ΠΎΠΊΠΎ Π² Π±ΡΠ΄ΡΡΠ΅ΠΌ.ΠΠΎΡΠ»ΡΠ΄ΠΆΡΠ²Π°Π»ΠΈΡΡ ΠΌΠ΅Ρ
Π°Π½ΡΠ·ΠΌΠΈ Π΄ΡΡ Π°Π½ΡΠΈΠΎΠΊΡΠΈΠ΄Π°Π½ΡΡΠ² Π½Π° Π·Π°ΠΏΠΎΠ±ΡΠ³Π°Π½Π½Ρ ΡΠΎΠ·Π²ΠΈΡΠΊΡ
ΠΊΠ°ΡΠ°ΡΠ°ΠΊΡΠΈ Ρ ΠΊΡΡΡΡΠΈΡ
. ΠΠΈΡΠ°ΡΡ ΠΊΡΠΈΡΡΠ°Π»ΠΈΠΊΠΈ Π±ΡΠ»ΠΈ Π²ΠΈΡΡΠΈΠΌΠ°Π½Ρ Π² ΠΊΡΠ»ΡΡΡΡΠ°Π»ΡΠ½ΠΎΠΌΡ
ΡΠ΅ΡΠ΅Π΄ΠΎΠ²ΠΈΡΡ, ΡΠΎ ΠΌΡΡΡΠΈΡΡ 450 ΠΌΠ³ Π³Π»ΡΠΊΠΎΠ·ΠΈ Π½Π° 100 Π³ ΡΠΎΠ·ΡΠΈΠ½Ρ Ρ Π· Π°Π½ΡΠΈΠΎΠΊΠΈΡΠ»ΡΠ²Π°ΡΠ°ΠΌΠΈ - Π΄Π΅ΡΡΠ΅ΡΠΎΠΊΡΠ°ΠΌΡΠ½ΠΎΠΌ (DFO) Ρ N-Π°ΡΠ΅ΡΠΈΠ»-L-ΡΠΈΡΡΠ΅ΡΠ½ΠΎΠΌ (NAC) ΠΏΡΠΎΡΡΠ³ΠΎΠΌ 12 Π΄Π½ΡΠ².
Π’Π°ΠΊ ΡΠ°ΠΌΠΎ 4 Π΄Π½Ρ Π»ΡΠ½Π·ΠΈ ΠΌΡΡΡΠΈΠ»ΠΈΡΡ Π² ΠΊΡΠ»ΡΡΡΡΠ°Π»ΡΠ½ΠΎΡ ΡΠ΅ΡΠ΅Π΄ΠΎΠ²ΠΈΡΡ, Π½Π°ΡΠΈΡΡΡ ΡΠΈΠ³Π°ΡΠΊΠΎΠ²ΠΈΠΌ Π΄ΠΈΠΌΠΎΠΌ, ΡΠΎΠ΄Π΅Π½Π½Π° Π΄ΠΎΠ·Π° ΡΠΊΠΎΠ³ΠΎ ΡΡΠ°Π½ΠΎΠ²ΠΈΠ»Π° 500 psi. ΠΠΏΡΠΈΡΠ½Π° ΡΠΊΡΡΡΡ ΠΊΡΠΈΡΡΠ°Π»ΠΈΠΊΡΠ² ΡΠΎΠ΄Π½Ρ ΠΎΡΡΠ½ΡΠ²Π°Π»ΠΎΡΡ Π·Π° Π΄ΠΎΠΏΠΎΠΌΠΎΠ³ΠΎΡ
Π»Π°Π·Π΅ΡΠ½ΠΎΡ ΡΡΡΠ°Π½ΠΎΠ²ΠΊΠΈ. ΠΠ°ΠΏΡΠΈΠΊΡΠ½ΡΡ ΡΠ½ΠΊΡΠ±Π°ΡΡΠΉΠ½ΠΎΠ³ΠΎ ΠΏΠ΅ΡΡΠΎΠ΄Ρ ΠΊΡΠΈΡΡΠ°Π»ΠΈΠΊΠΈ Π±ΡΠ»ΠΈ Π²ΠΈΠ²ΡΠ΅Π½Ρ
ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΡΠ½Π²Π΅ΡΡΡΠΉΠ½ΠΎΡ ΠΌΡΠΊΡΠΎΡΠΊΠΎΠΏΡΡ, a Π΅ΠΏΡΡΠ΅Π»ΡΠ°Π»ΡΠ½ΠΈΠΉ ΡΠ°Ρ Π²ΠΈΠΊΠΎΡΠΈΡΡΠΎΠ²ΡΠ²Π°Π²ΡΡ Π΄Π»Ρ Π³ΠΈΡΡΠΎΡ
ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΌΠ΅ΡΠΎΠ΄Ρ ΠΎΡΡΠ½ΠΊΠΈ Π½ΡΠΊΠ»Π΅ΡΠ½ΠΎΠ²ΠΈx
ΠΊΠΈΡΠ»ΠΎΡ ΡΠ°ΡΠ±ΡΠ²Π°Π½Π½ΡΠΌ ΠΠΠ-Π ΠΠ ΠΏo ΠΌΠ΅ΡΠΎΠ΄Ρ ΠΠΉΠ½Π°ΡΡΠΎΠ½Π°. ΠΠΊΡΠΈΠ²Π½Ρ ΡΠΎΡΠΌΠΈ ΠΊΠΈΡΠ½Ρ
(ROS) Π±ΡΠ»ΠΈ ΠΎΡΡΠ½Π΅Π½Ρ Π² Π΅ΠΏΡΡΠ΅Π»ΡΠ°Π»ΡΠ½ΠΈΡ
ΠΊΠ»ΡΡΠΈΠ½Π°Ρ
ΠΊΡΠΈΡΡΠ°Π»ΠΈΠΊΠ° Π·Π° Π΄ΠΎΠΏΠΎΠΌΠΎΠ³ΠΎΡ
ΡΠ»yΠΎΡΠ΅ΡΡΠ΅Π½ΡΠ½ΠΎΠΉ ΠΌΡΠΊΡΠΎΡΠΊΠΎΠΏΡΡ Π΄Π»Ρ Π²ΠΈΠΌΡΡΡ
ΡΡΠ²Π½Ρ ΠΊΠ»ΡΡΠΈΠ½Π½ΠΎΠ³ΠΎ ΠΎΠΊΠΈΡΠ»Π΅Π½Π½Ρ ΡΠΎΠ΄ΠΎ ΠΊΡΠ»ΡΡΡΡ
ΠΊΠΎΠ½ΡΡΠΎΠ»Ρ. ΠΠΈΡΠΎΠΊΠ° Π΄ΠΎΠ·Π° Π³Π»ΡΠΊΠΎΠ·ΠΈ Π· Π΄ΠΈΠΌΠΎΠΌ
Π²ΠΈΠΊΠ»ΠΈΠΊΠ°Ρ ΠΎΠΏΡΠΈΡΠ½Ρ ΡΠ° ΠΌΠΎΡΡΠΎΠ»ΠΎΠ³ΡΡΠ½Ρ Π·ΠΌΡΠ½ΠΈ
Π² Π΅ΠΏΡΡΠ΅Π»ΡΠ°Π»ΡΠ½ΠΈΡ
ΠΊΠ»ΡΡΠΈΠ½Π°Ρ
(Π³ΡΠΏΠ΅ΡΡΡΠΎΡΡΡ,
Π³ΡΠΏΠ΅ΡΠΏΠ»Π°Π·ΡΡ) Ρ Π·Π±ΡΠ»ΡΡΡΡ ΡΠ»yΠΎΡΠ΅ΡΡΠ΅Π½ΡΡΡ.
ΠΠ½ΡΠΈΠΎΠΊΡΠΈΠ΄Π°Π½ΡΠΈ Π·ΠΌΠ΅Π½ΡΡΡΡΡ ΡΠ΅ΠΉ Π²ΠΏΠ»ΠΈΠ²,
Π·Π½ΠΈΠΆΡΡΡΡ ΠΊΡΠ»ΡΠΊΡΡΡΡ ΠΏΠΎΡΠΊΠΎΠ΄ΠΆΠ΅Π½ΠΈΡ
ΠΊΠ»ΡΡΠΈΠ½,
Π·Π°ΠΏΠΎΠ±ΡΠ³Π°ΡΡΡ Π·Π±ΡΠ»ΡΡΠ΅Π½Ρ Π΄ΡΡΠ»ΡΠ½ΡΡΡΡ ROS.
NAC Π·Π°Ρ
ΠΈΡΡΠΈΠ² Π»ΡΠ½Π·ΠΈ Π²ΡΠ΄ ΠΏΠΎΡΠΊΠΎΠ΄ΠΆΠ΅Π½Π½Ρ
Π΄Π΅ΡΠΎ ΠΊΡΠ°ΡΠ΅, Π½ΡΠΆ DFO. ΠΠΈ ΠΏΡΠΈΠΏΡΡΠΊΠ°ΡΠΌΠΎ,
ΡΠΎ Π΄Π°Π½Ρ Π°Π½ΡΠΈΠΎΠΊΠΈΡΠ»ΡΠ²Π°ΡΡ ΠΌΠΎΠΆΡΡΡ ΡΠ»ΡΠΆΠΈΡΠΈ
Π΅ΡΠ΅ΠΊΡΠΈΠ²Π½ΠΈΠΌ Π·Π°ΡΠΎΠ±ΠΎΠΌ Π·Π°Ρ
ΠΈΡΡΡ ΠΊΡΠΈΡΡΠ°Π»ΠΈΠΊΠ° ΠΎΠΊΠ° ΠΏΡΠΎΡΠΈ ΠΏΠΎΡΠΊΠΎΠ΄ΠΆΠ΅Π½Π½Ρ Ρ ΠΊΡΡΡΡΠΈΡ
Π΄ΡΠ°Π±Π΅ΡΠΈΠΊΡΠ². Π’Π°ΠΊΠΈΠΌ ΡΠΈΠ½ΠΎΠΌ, Π·Π°ΡΡΠΎΡΡΠ²Π°Π½Π½Ρ Π°Π½ΡΠΈΠΎΠΊΠΈΡΠ½ΠΈΡ
ΡΠ΅ΡΠΎΠ²ΠΈΠ½ Π² ΠΏΡΠΎΡΡΠ»Π°ΠΊΡΠΈΡΡ ΠΊΠ°ΡΠ°ΡΠ°ΠΊΡΠΈ y ΠΊΡΡΡΡΠ² ΡΠ° Π»ΡΠΊΡΠ²Π°Π½Π½Ρ Π΄ΡΠΆΠ΅ ΠΏΡΠΈΠ²Π°Π±Π»ΠΈΠ²Π° ΠΌΠΎΠΆΠ»ΠΈΠ²ΡΡΡΡ, ΡΠΊΠ° ΠΌΠΎΠΆΠ΅ Π±ΡΡΠΈ Π΄ΠΎΡΠ»ΡΠ΄ΠΆΠ΅Π½ΠΎΡ Π±ΡΠ»ΡΡ Π³Π»ΠΈΠ±ΠΎΠΊΠΎ Π² ΠΌΠ°ΠΉΠ±ΡΡΠ½ΡΠΎΠΌΡ
Antiradical effects in l-propionyl carnitine protection of the heart against ischemia-reperfusion injury: The possible role of iron chelation
l-Propionyl carnitine has been shown to improve the heart's mechanical recovery and other metabolic parameters after ischemia-reperfusion. However, the mechanism of protection is unknown. The two dominating hypotheses are: (i) l-propionyl carnitine can serve as an energy source for heart muscle cells by being enzymatically converted to propionyl-CoA and subsequently utilized in the Krebs cycle (a metabolic hypothesis), and (ii) it can act as an antiradical agent, protecting myocardial cells from oxidative damage (a free radical hypothesis). To test the two possible pathways, we compared the protection afforded to the ischemia-reperfused hearts by l-propionyl carnitine and its optical isomer, d-propionyl carnitine. The latter cannot be enzymatically utilized as an energy source. The Langendorff perfusion technique was used and the hearts were subjected to 40 min of ischemia and 20 min of reperfusion. In analysis of ischemiareperfused hearts, a strong correlation was found between the recovery of mechanical function and the presence of protein oxidation products (protein carbonyls). Both propionyl carnitines efficiently prevented protein oxidation but l-propionyl carnitine-perfused hearts had two times greater left ventricular developed pressure. The results indicate that both metabolic and antiradical pathway are involved in the protective mechanism of l-propionyl carnitine. To obtain a better insight of the antiradical mechanism of l-propionyl carnitine, we compared the ability of l- and d-propionyl carnitines, l-carnitine, and deferoxamine to interact with: (i) peroxyl radicals, (ii) oxygen radicals, and (iii) iron. We found that none of the carnitine derivatives were able to scavenge peroxyl radicals or superoxide radicals. l- and d-propionyl carnitine and deferoxamine (not l-carnitine) suppressed hydroxyl radical production in the Fenton system, probably by chelating the iron required for the generation of hydroxyl radicals. We suggest that l-propionyl carnitine protects the heart by a dual mechanism: it is an efficient fuel source and an antiradical agent
Modulation of cutaneous wound healing by ozone: differences between young and aged mice.
Cutaneous tissues are frequently exposed to prooxidative environments, including UV radiation and air pollutants. Among the latter, ozone (O(3)) is of particular concern because of its high and dominating presence in photochemical smog. It is well known that O(3) depletes small molecular weight antioxidants, oxidizes proteins, induces lipid peroxidation and activates cellular responses in various tissues. Using an in vivo model (SKH-1 hairless mice), the interaction between O(3) exposure (0.5ppmx6h/day) and age was examined in relation to cutaneous wound healing. Compared to younger (8 weeks) mice, older (18 months) mice exposed to O(3) (day 0 to day 9 after wounding) exhibited delayed wound closure, increased lipid peroxidation (measured as 4-HNE protein adducts) and protein oxidation (measured as carbonyls concentration) and decreased levels of P-IkappaBalpha and TGFbeta protein. These findings support the hypothesis that oxidant pollutant exposure and age interact so as to disrupt normal wound healing processes