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1.
Braz J Med Biol Res ; 49(6): e5116, 2016.
Article in English | MEDLINE | ID: mdl-27254659

ABSTRACT

Supraphysiological administration of anabolic androgenic steroids has been linked to increased blood pressure. The widely distributed amino acid taurine seems to be an effective depressor agent in drug-induced hypertension. The purpose of this study was to assess the impact of chronic high dose administration of nandrolone decanoate (DECA) and taurine on blood pressure in rats and to verify the potentially involved mechanisms. The study was conducted in 4 groups of 8 adult male Wistar rats, aged 14 weeks, treated for 12 weeks with: DECA (A group); vehicle (C group); taurine (T group), or with both drugs (AT group). Systolic blood pressure (SBP) was measured at the beginning of the study (SBP1), 2 (SBP2) and 3 months (SBP3) later. Plasma angiotensin-converting enzyme (ACE) activity and plasma end products of nitric oxide metabolism (NOx) were also determined. SBP3 and SBP2 were significantly increased compared to SBP1 only in the A group (P<0.002 for both). SBP2, SBP3 and ACE activity showed a statistically significant increase in the A vs C (P<0.005), andvs AT groups (P<0.05), while NOx was significantly decreased in the A and AT groups vs controls (P=0.01). ACE activity was strongly correlated with SBP3 in the A group (r=0.71, P=0.04). These findings suggest that oral supplementation of taurine may prevent the increase in SBP induced by DECA, an effect potentially mediated by angiotensin-converting enzyme.


Subject(s)
Anabolic Agents/administration & dosage , Blood Pressure/drug effects , Nandrolone/analogs & derivatives , Taurine/administration & dosage , Anabolic Agents/adverse effects , Animals , Hypertension/chemically induced , Hypertension/prevention & control , Male , Nandrolone/administration & dosage , Nandrolone/adverse effects , Nandrolone Decanoate , Nitrates/blood , Nitric Oxide/metabolism , Nitrites/blood , Peptidyl-Dipeptidase A/blood , Random Allocation , Rats, Wistar , Reference Values , Spectrophotometry/methods , Time Factors
2.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;49(6): e5116, 2016. tab, graf
Article in English | LILACS | ID: biblio-951683

ABSTRACT

Supraphysiological administration of anabolic androgenic steroids has been linked to increased blood pressure. The widely distributed amino acid taurine seems to be an effective depressor agent in drug-induced hypertension. The purpose of this study was to assess the impact of chronic high dose administration of nandrolone decanoate (DECA) and taurine on blood pressure in rats and to verify the potentially involved mechanisms. The study was conducted in 4 groups of 8 adult male Wistar rats, aged 14 weeks, treated for 12 weeks with: DECA (A group); vehicle (C group); taurine (T group), or with both drugs (AT group). Systolic blood pressure (SBP) was measured at the beginning of the study (SBP1), 2 (SBP2) and 3 months (SBP3) later. Plasma angiotensin-converting enzyme (ACE) activity and plasma end products of nitric oxide metabolism (NOx) were also determined. SBP3 and SBP2 were significantly increased compared to SBP1 only in the A group (P<0.002 for both). SBP2, SBP3 and ACE activity showed a statistically significant increase in the A vs C (P<0.005), andvs AT groups (P<0.05), while NOx was significantly decreased in the A and AT groups vs controls (P=0.01). ACE activity was strongly correlated with SBP3 in the A group (r=0.71, P=0.04). These findings suggest that oral supplementation of taurine may prevent the increase in SBP induced by DECA, an effect potentially mediated by angiotensin-converting enzyme.


Subject(s)
Animals , Male , Blood Pressure/drug effects , Anabolic Agents/administration & dosage , Nandrolone/analogs & derivatives , Reference Values , Time Factors , Random Allocation , Anabolic Agents/adverse effects , Hypertension/chemically induced , Hypertension/prevention & control , Nandrolone/administration & dosage
3.
J Med Life ; 8 Spec Issue: 69-73, 2015.
Article in English | MEDLINE | ID: mdl-26361515

ABSTRACT

Introduction Intravenous iron administration in patients treated by haemodialysis for end stage renal disease can exacerbate oxidative stress by increasing the level of free redox active iron. A way to reduce the impact of iron on oxidative stress in haemodialysis patients may be the administration of iron through arterial extracorporeal circuit. Objective The aim of our study was to compare the influence of iron route of administration (venous versus arterial extracorporeal circuit infusion) on antioxidant parameters in red blood cells of haemodialysis patients in order to clarify if arterial iron administration can have positive impacts related to iron induced oxidative stress. Method Twenty stable patients on regular haemodialysis treatment were selected for the study. They were investigated in a cross-over design at 3 mid-week HD sessions, one week apart, without iron [HD basal] and with either IV infusion of 100mg iron sucrose over the first 20 minutes of HD session, via venous line [HDvenous], or the same solution infused on the arterial extracorporeal circulation [HDarterial]. Blood samples were drawn at 0 min, 40 min and 270 min. Erythrocytes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) activity, non-protein thiol levels and total antioxidant capacity (TEAC) were analysed. Conclusion Haemodialysis significantly decreases the total antioxidant activity in erythrocytes. Iron supplementation, through venous or arterial extracorporeal route has no impact on the total antioxidant activity in red blood cells. Venous iron administration increases GPx activity in erythrocytes suggesting increased lipid peroxidation compared with arterial extracorporeal administration.


Subject(s)
Antioxidants/metabolism , Catalase/metabolism , Erythrocytes/metabolism , Iron/administration & dosage , Iron/pharmacology , Renal Dialysis , Superoxide Dismutase/metabolism , Erythrocytes/drug effects , Erythrocytes/enzymology , Glutathione Peroxidase/metabolism , Humans , Injections, Intra-Arterial , Injections, Intravenous , Sulfhydryl Compounds/metabolism
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