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Effect of N-acetylcysteine administration on homocysteine level and oxidative damage to proteins in lead-exposed workers
onic sympathetic nerve fibres innervating the resistance vessels or by intravenous injection of phenylephrine (10 nmol/kg). Acute HF was induced by transverse aortic constriction (TAC) immediately after S1. Basal SBP before S1 was 66.9 ± 1.7 mmHg (n = 21). It was increased (S1) by 42.0 ± 3.0 (n=10) and 48.6 ± 4.7 mmHg (n = 10) by electrical and chemical stimulation, respectively. TAC or vasopressin infusion (in sham operated rats) elevated basal SBP to 175.8 ± 4.5 mmHg (n = 10) and to 173.0 ± 4.2 (n = 11), respectively. The electrically-stimulated increases in
SBP (S2–S4 applied 15 min after TAC in 10 min intervals) were reduced by about 50% in TAC but not in sham operated rats. On the contrary, the phenylephrine-induced vasopressor responses did not markedly change in S1–S4 both in TAC and sham-operated rats. Our results demonstrate that acute heart failure inhibits the neurogenic vasopressor response via (a) presynaptic mechanism(s). However, the precise presynaptic receptor type(s) involved in this inhibition remain(s) to be established.
Effect of N-acetylcysteine administration on homocysteine level and oxidative damage to proteins in lead-exposed workers S³awomir Kasperczyk1, Micha³ Dobrakowski1, Aleksandra Kasperczyk1, Ewa Romuk1, Natalia Pawlas2, Ewa Birkner1 Department
of Biochemistry, Medical University of Silesia, Jordana 19, PL 41-808 Zabrze, Poland; Department of Chemical Hazards and Genetic Toxicology, Institute of Occupational Medicine and Environmental Health, Koœcielna 13, PL 41-200 Sosnowiec, Poland
The aim of the study was to investigate the influence of N-acetylcysteine (NAC) administration on homocysteine level and oxidative damage to proteins in lead-exposed workers. The examined population (n = 171) was composed of male employees who worked with lead and were randomized into four groups. Workers who were not administered any antioxidants, drugs, vitamins or dietary supplements were classified as the reference group (n = 49). The remaining three groups consisted of workers who were treated with NAC in three different doses for 12 weeks (200, 400, 800 mg).
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Pharmacological Reports, 2013, 65, suppl.
After treatment, blood lead levels significantly decreased in the groups receiving NAC compared to the reference group. Homocysteine levels significantly decreased or showed a strong tendency toward lower values depending on the NAC dose. Levels of protein carbonyl groups were significantly decreased in all groups receiving NAC, while level of thiol groups was significantly elevated in the group receiving 200 mg of NAC. Treatment with NAC normalizes level of homocysteine and decreases oxidative stress measured as protein carbonyl content in a dose-dependent manner.
SBP (S2–S4 applied 15 min after TAC in 10 min intervals) were reduced by about 50% in TAC but not in sham operated rats. On the contrary, the phenylephrine-induced vasopressor responses did not markedly change in S1–S4 both in TAC and sham-operated rats. Our results demonstrate that acute heart failure inhibits the neurogenic vasopressor response via (a) presynaptic mechanism(s). However, the precise presynaptic receptor type(s) involved in this inhibition remain(s) to be established.
Effect of N-acetylcysteine administration on homocysteine level and oxidative damage to proteins in lead-exposed workers S³awomir Kasperczyk1, Micha³ Dobrakowski1, Aleksandra Kasperczyk1, Ewa Romuk1, Natalia Pawlas2, Ewa Birkner1 Department
of Biochemistry, Medical University of Silesia, Jordana 19, PL 41-808 Zabrze, Poland; Department of Chemical Hazards and Genetic Toxicology, Institute of Occupational Medicine and Environmental Health, Koœcielna 13, PL 41-200 Sosnowiec, Poland
The aim of the study was to investigate the influence of N-acetylcysteine (NAC) administration on homocysteine level and oxidative damage to proteins in lead-exposed workers. The examined population (n = 171) was composed of male employees who worked with lead and were randomized into four groups. Workers who were not administered any antioxidants, drugs, vitamins or dietary supplements were classified as the reference group (n = 49). The remaining three groups consisted of workers who were treated with NAC in three different doses for 12 weeks (200, 400, 800 mg).
54
Pharmacological Reports, 2013, 65, suppl.
After treatment, blood lead levels significantly decreased in the groups receiving NAC compared to the reference group. Homocysteine levels significantly decreased or showed a strong tendency toward lower values depending on the NAC dose. Levels of protein carbonyl groups were significantly decreased in all groups receiving NAC, while level of thiol groups was significantly elevated in the group receiving 200 mg of NAC. Treatment with NAC normalizes level of homocysteine and decreases oxidative stress measured as protein carbonyl content in a dose-dependent manner.