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Antioxidative Mechanisms (antioxidative + mechanism)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

FK506 and Sildenafil Promote Erectile Function Recovery after Cavernous Nerve Injury Through Antioxidative Mechanisms

THE JOURNAL OF SEXUAL MEDICINE, Issue 4i 2007
Gwen Lagoda MS
ABSTRACT Introduction., Immunophilin ligands and phosphodiesterase type 5 (PDE5) inhibitors are touted to promote erectile function recovery after cavernous nerve (CN) injury. However, the mechanisms for their effects remain unclear. Aim., To compare the erection recovery effects of the immunophilin ligand FK506 and the PDE5 inhibitor sildenafil after CN injury and determine whether they involve antioxidative and/or antiapoptotic mechanisms. Methods., Initial experiments established conditions of our CN injury model in adult male Sprague-Dawley rats. Subsequently, we evaluated treatment effects 14 days after: (i) unilateral CN injury (UNI) + saline (vehicle control); (ii) UNI + FK506 (5 mg/kg once daily, subcutaneous ×5 days); (iii) UNI + sildenafil (20 mg/kg every 8 hours, subcutaneous ×7 days); (iv) UNI + FK506/sildenafil; and (v) sham surgery. Main Outcome Measures., Intracavernous pressure (ICP) measurement after CN electrical stimulation to assess erectile function and Western blot analysis of expressions of glutathione peroxidase (GPX; antioxidant enzyme), nitrotyrosine (NT; oxidative stress marker), and phosphorylated and total Akt (antiapoptotic factor) in penes. Results., In the UNI model, GPX expression was increased at Days 1 and 7, while p-Akt expression decreased at Day 1 and returned to baseline at Day 7. GPX expression was significantly higher in the UNI + FK506 group compared with the saline-treated group (P < 0.05). ICP increased in all treatment groups compared with that of the saline-treated group (P < 0.05). NT levels were increased after saline treatment (P < 0.05) but not after FK506 and sildenafil treatment, alone or in combination. GPX was localized to nerves coursing through the penis and to smooth muscle and endothelium of the dorsal vein and arteries. Conclusions., Both FK506 and sildenafil protect erectile function after CN injury by decreasing oxidative stress-associated tissue damage. FK506 may act through increased GPX activity. Further research is required to elucidate mechanisms associated with the beneficial effect of sildenafil. Lagoda G, Jin L, Lehrfeld TJ, Liu T, and Burnett AL. FK506 and sildenafil promote erectile function recovery after cavernous nerve injury through antioxidative mechanisms. J Sex Med 2007;4:908,916. [source]

Kinetic Study of the Quenching Reaction of Singlet Oxygen by Common Synthetic Antioxidants (tert -Butylhydroxyanisol, tert -di-Butylhydroxytoluene, and tert -Butylhydroquinone) as Compared with ,-Tocopherol

JOURNAL OF FOOD SCIENCE, Issue 5 2009
Ji In Kim
ABSTRACT:, Effects of synthetic phenolic antioxidants (BHA, BHT, and TBHQ) on the methylene blue (MB) sensitized photooxidation of linoleic acid as compared with that of ,-tocopherol have been studied. Their antioxidative mechanism was studied by both ESR spectroscopy in a 2,2,6,6-tetramethylpiperidone (TMPD)-methylene blue (MB) system and spectroscopic analysis of rubrene oxidation induced by a chemical source of singlet oxygen. Total singlet oxygen quenching rate constants (kox,Q+kq) were determined using a steady state kinetic equation. TBHQ showed the strongest protective activity against the MB sensitized photooxidation of linoleic acid, followed by BHA and BHT. TBHQ (1 × 10,3 M) exhibited 86.5% and 71.4% inhibition of peroxide and conjugated diene formations, respectively, in linoleic acid photooxidation after 60-min light illumination. The protective activity of TBHQ against the photosensitized oxidation of linoleic acid was almost comparable to that of ,-tocopherol. The data obtained from ESR and rubrene oxidation studies clearly showed the strong singlet oxygen quenching ability of TBHQ. The kox,Q+kq of BHA, BHT, and TBHQ were determined to be 3.37 × 107, 4.26 × 106, and 1.67 × 108 M,1 s,1, respectively. The kox,Q+kq of TBHQ was within the same order of magnitude of that of ,-tocopherol, a known efficient singlet oxygen quencher. There was a high negative correlation (r2,=,,0.991) between log (kox,Q+kq) and reported oxidation potentials for the synthetic antioxidants, indicating their charge-transfer mechanism for singlet oxygen quenching. This is the 1st report on the kinetic study on kox,Q+kq of TBHQ in methanol as compared with other commonly used commercial synthetic antioxidants and ,-tocopherol. [source]

Effects of isoflurane on nitric oxide metabolism and oxidant status of guinea pig myocardium

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 1 2001
. Durak
Background: Volatile anesthetics (VAs) have been shown to enhance myocardial recovery during reperfusion, the mechanism of which has not been clarified yet. It has been supposed that this effect of VAs may appear through antioxidative mechanisms. Methods: Thirty guinea pigs were used in the study. There were three groups with 10 animals in each: I , control, II , isoflurane+oxygen and III , oxygen. Isoflurane (2.0% v/v) and oxygen (100%) mixture was given to the animals via a face mask in the isoflurane+oxygen group at the rate of 2 l per min for 30 min a day for three consecutive days. In the oxygen group, oxygen alone (100%) was given under the same conditions as in the isoflurane+oxygen group. At the end of the experiments, the animals were killed and their hearts were removed. In the heart tissues, nitric oxide synthase (NOS) activity, nitric oxide (NO) pool (NO,+NO2,) and malondialdehyde (MDA) levels were measured. Results: NOS activity was found to be higher and the NO pool lower in the isoflurane+oxygen group compared with those of control and oxygen groups. In the oxygen group, MDA level was found to be higher compared to the other groups. There was, however, no significant difference between MDA levels of the control and isoflurane+oxygen groups. Conclusion: Our results suggest that isoflurane prevents peroxidation reactions in heart tissue, possibly by scavenging toxic oxygen radicals produced under hyperoxygenation conditions as occurs with general anesthesia. [source]