Eight male volunteers, all alcohol addicts selected from the patients of the Pădureni unit, deprived for a minimum of two weeks of alcohol, but with an at least 2-year history of alcohol addiction, received 0.5 ml absolute alcohol/kg body weight. Following dynamically the alteration of plasma reduced glutathione content, a significant increase (+8.27%) 30 minutes after alcohol ingestion and a decrease (-7.02%) before ingestion, as compared to plasma glutathione level in sex and age-matched clinically normal subject (100%) was noticed. The change in the --SH groups content in plasma after chronic alcohol ingestion leads to the occurrence of cell oxidative stress, as well as to a decreased resistance of hepatic cell and whole body as a result of the lipid peroxidation process and/or occurrence of detrimental reactive radical species, issuing from O2.

Adult↗

PubMedDate not supplied

Possible involvement of the L-arginine-nitric oxide pathway in the modulation of stress-induced analgesia.

The possible participation of nitric oxide (NO) in pain modulation and stress analgesia was studied in adult Wistar rats. Cerebral citruline as a coproduct of NO from L-arginine increased from the mean value 5.6 +/- 0.4 nM/mg.Pt. to 8.9 +/- 0.5 nM/mg.Pt. in acute restraint stress. In high doses (50 mg/kg body weight), intraperitoneal administration of L-arginine caused a small and transient decrease of the tail-flick latencies to the thermal stimulus, without significant changes of the stress analgesia induced by restraint stress. In animals pretreated with N-nitro-L-arginine methyl ester (NAME) a progressive increase of the latency time was obtained and the increased latencies induced by acute immobilization appeared significantly potentiated. These results offer new indirect evidence in favour of the modulatory role of NO in thermoalgesic sensitivity and stress-induced analgesia.

Animals↗

PubMedDate not supplied

[The epidemiological and laboratory aspects of the risk factors for essential arterial hypertension in adults in a rural area].

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Adult↗

PubMedDate not supplied

[Glutathione, a biochemical indicator for different types of cellular stress. The change in the GSH level in the brain of rats with hypoxia].

By the ligation of left vertebral artery in some white, adult WISTAR rats, of 150-200 g, anaesthetized with ether, a cerebral hypoxia of 10 minutes was induced. After beheading, there was determined the level of SH-neproteic groups and glutathione (GSH) in the whole heparinized blood and there was observed an important decrease with -15.88% and -16.80% respectively, in comparison with the normal lot (100%), kept under the some laboratory conditions. The GSH level in the neural cytosol is also significantly decreased with -8.66% in rats with hypoxia. The GSH depletion in the induced hypoxia, by our experiment, might be due to the reaction between nitric oxide (NO.) radical and intracellular GSH (blood and neuronal cytosol), considering the literature in this field, and S-nitrosoglutathion (S-NO-GSH) bioactive intermediary is formed and it protects the hypoxied brain against the NO.-dependent cytotoxicity, in the initial phase of hypoxia. The decrease of GSH and SH-neproteic groups level is considered a biochemical marker of the growth of the free radicals level to O2 (NO., O2., OH., H2O2, 1O2), that appear in the hypoxic and/or ischemic stress, but also a major sign in the rol of "scavenger" and antioxidant of the radicals at the cerebral and sanguine level, in the above mentioned conditions.

Animals↗

PubMedDate not supplied

Possible involvement of L-arginine-nitric oxide pathway in the modulation of stress-induced analgesia.

The possible participation of NO in the pain modulation and stress analgesia was studied in Wistar adult rats. Cerebral citruline as a stoichiometric coproduct of NO from L-arginine increased from the mean value 5.6 +/- 0.4 nM/mg.Pt. to 8.9 +/- 0.5 nM/mg.Pt. in acute immobilization stress. Intraperitoneal administration of L-arginine caused only in high doses (50 mg/kg body weight) a small transient decrease of tail-flick latencies to the thermoalgesic stimulus, without significant changes of the stress analgesia induced by the restraint stress. In the pretreated animals with L-NAME a progressive increase of latency time was obtained and the increased latencies induced by acute immobilization appeared significantly potentiated. These results offer new indirect evidence in favour of the modulatory role of NO in the thermoalgesic sensitivity and stress induced analgesia.

Analgesia↗