The Induction of Oxidative/Nitrosative Stress, Inflammation, and Apoptosis by a Ferric Carboxymaltose Copy Compared to Iron Sucrose in a Non-Clinical Model

Introduction: Ferric carboxymaltose is a next-generation polynuclear iron(III)-hydroxide carbohydrate complex for intravenous iron therapy belonging to the class of so-called non-biological complex drugs. The product characteristics and therapeutic performance of non-biological complex drugs are largely defined by the manufacturing process. A follow-on product, termed herein as ferric carboxymaltose similar, is available in India. Given that non-biological complex drugs may display differences in diverse product properties not characterisable by physico-chemical methods alone. Aim: The aim is to assess the effects of this ferric carboxymaltose similar in our non-clinical model in non-anaemic healthy rats. Materials and Methods: Non-anaemic rats were treated with intravenous ferric carboxymaltose similar or iron sucrose both at (40 mg iron/kg body weight), or with saline solution (control) for four weeks, after which the animals were sacrificed. Parameters for tissue iron distribution, oxidative stress, nitrosative stress, inflammation and apoptosis were assessed by immunohistomorphometry. Results: Ferric carboxymaltose similar resulted in deranged iron distribution versus iron sucrose originator as indicated by increased serum iron, transferrin saturation and tissue iron(III) deposits as well as decreased ferritin deposits in the liver, heart and kidneys versus iron sucrose originator. Ferric carboxymaltose similar also increased significantly oxidative/nitrosative stress, pro-inflammatory, and apoptosis markers in the liver, heart and kidneys versus iron sucrose originator. Conclusion: In our rat model, ferric carboxymaltose similar had a less favourable safety profile than iron sucrose originator, adversely affecting iron deposition, oxidative and nitrosative stress, inflammatory responses, with impaired liver and kidney function.Fil: Toblli, Jorge Eduardo. Hospital Alemán; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Cao, Gabriel Fernando. Hospital Alemán; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Angerosa, Margarita. Hospital Alemán; Argentin

Comparison of Oxidative Stress and Inflammation Induced by Different Intravenous Iron Sucrose Similar Preparations in a Rat Model

Iron sucrose originator (ISORIG) has been used to treat iron deficiency and iron deficiency anemia for decades. Iron sucrose similars (ISSs) have recently entered the market. In this non-clinical study of non-anemic rats, five doses (40 mg iron/kg body weight) of six ISSs marketed in Asian countries, ISORIG or saline solution (control) were administered intravenously over four weeks to compare their toxicologic effects. Vasodilatory effects, impaired renal function and hepatic damage were only observed in the ISS groups. Significantly elevated serum iron and transferrin saturation levels were observed in the ISS groups suggesting a higher release of iron resulting in higher amounts of non-transferrin bound (free) iron compared to ISORIG. This might explain the elevated oxidative stress and increased levels of inflammatory markers and antioxidant enzymes in the liver, heart and kidneys of ISS-treated animals. Physico-chemical analyses showed that the molecular structure of most of the ISSs differed greatly from that of the ISORIG. These differences may be responsible for the organ damage and oxidative stress observed in the ISS groups. Significant differences were also found between different lots of a single ISS product. In contrast, polarographic analyses of three different ISORIG lots were identical, indicating that the molecular structure and thus the manufacturing process for ISORIG is highly consistent. Data from this study suggest that ISSs and ISORIG differ significantly. Therefore, before widespread use of these products it would be prudent to evaluate additional non-clinical and/or clinical data proving the safety, therapeutic equivalence and interchangeability of ISSs with ISORIG

Effects of iron deficiency anemia and its treatment with iron polymaltose complex in pregnant rats, their fetuses and placentas: Oxidative stress markers and pregnancy outcome

Objective: Iron deficiency anemia (IDA) can severely impair the outcome of pregnancy. IDA has been shown to cause oxidative stress, which may be exacerbated by oral iron therapy. In this study, the effects of IDA and its treatment with iron polymaltose complex/folic acid (IPC/FA) were examined in anemic pregnant rats, their fetuses and placentas. Study design: Hematological variables and oxidative stress markers in the liver, heart and kidney were evaluated in non-anemic, anemic and IPC/FA-treated pregnant rats and their fetuses. Markers for oxidative stress, inflammation and hypoxia were assessed in the placentas of all groups. Results: IDA was shown to increase oxidative stress levels in all the studied organs and in placenta as well as hypoxia and inflammation in placenta. IPC/FA treatment corrected IDA measured by the hemoglobin level, serum iron level and transferrin saturation. The oxidative stress levels in all the studied organs and in placentas of the IPC/FA-treated group were comparable to those of the non-anemic group. The number of fetuses and the neonatal and placental weight were lower in the anemic group compared to the non-anemic and IPC/FA-treated groups. Conclusions: The current study shows that IDA in pregnant rats impaired pregnancy outcome, increased the expression of hypoxia and inflammatory markers in the placenta, and increased oxidative stress in dams, fetuses and placentas. Treatment with oral IPC/FA corrected the IDA as well as reduced the levels of oxidative stress and inflammatory markers close to non-anemic control values in all the studied organs.Fil: Toblli, Jorge Eduardo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Hospital Alemán; ArgentinaFil: Cao, Gabriel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Hospital Alemán; ArgentinaFil: Oliveri, L.. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Hospital Alemán; ArgentinaFil: Angerosa, M.. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Hospital Alemán; Argentin

Nebivolol: impact on cardiac and endothelial function and clinical utility

Endothelial dysfunction is a systemic pathological state of the endothelium characterized by a reduction in the bioavailability of vasodilators, essentially nitric oxide, leading to impaired endothelium-dependent vasodilation, as well as disarrangement in vascular wall metabolism and function. One of the key factors in endothelial dysfunction is overproduction of reactive oxygen species which participate in the development of hypertension, atherosclerosis, diabetes, cardiac hypertrophy, heart failure, ischemia-reperfusion injury, and stroke. Because impaired endothelial activity is believed to have a major causal role in the pathophysiology of vascular disease, hypertension, and heart failure, therapeutic agents which modify this condition are of clinical interest. Nebivolol is a third-generation β-blocker with high selectivity for β1-adrenergic receptors and causes vasodilation by interaction with the endothelial L-arginine/ nitric oxide pathway. This dual mechanism of action underscores several hemodynamic qualities of nebivolol, which include reductions in heart rate and blood pressure and improvements in systolic and diastolic function. Although nebivolol reduces blood pressure to a degree similar to that of conventional β-blockers and other types of antihypertensive drugs, it may have advantages in populations with difficult-to-treat hypertension, such as patients with heart failure along with other comorbidities, like diabetes and obesity, and elderly patients in whom nitric oxide-mediated endothelial dysfunction may be more pronounced. Furthermore, recent data indicate that nebivolol appears to be a cost-effective treatment for elderly patients with heart failure compared with standard care. Thus, nebivolol is an effective and well tolerated agent with benefits above those of traditional β-blockers due to its influence on nitric oxide release, which give it singular hemodynamic effects, cardioprotective activity, and a good tolerability profile. This paper reviews the pharmacology structure and properties of nebivolol, focusing on endothelial dysfunction, clinical utility, comparative efficacy, side effects, and quality of life in general with respect to the other antihypertensive agents

Immunohistochemical expression of intrarenal renin angiotensin system components in response to tempol in rats fed a high salt diet

AIM:To determine the effect of tempol in normal rats fed high salt on arterial pressure and the balance between antagonist components of the renal renin-angiotensin system.METHODS:Sprague-Dawley rats were fed with 8% NaCl high-salt (HS) or 0.4% NaCl (normal-salt, NS) diet for 3 wk, with or without tempol (T) (1 mmol/L, administered in drinking water). Mean arterial pressure (MAP), glomerular filtration rate (GFR), and urinary sodium excretion (UVNa) were measured. We evaluated angiotensin II (Ang II), angiotensin 1-7 (Ang 1-7), angiotensin converting enzyme 2 (ACE2), mas receptor (MasR), angiotensin type 1 receptor (AT1R) and angiotensin type 2 receptor (AT2R) in renal tissues by immunohistochemistry.RESULTS:The intake of high sodium produced a slight but significant increase in MAP and differentially regulated components of the renal renin-angiotensin system (RAS). This included an increase in Ang II and AT1R, and decrease in ACE-2 staining intensity using immunohistochemistry. Antioxidant supplementation with tempol increased natriuresis and GFR, prevented changes in blood pressure and reversed the imbalance of renal RAS components. This includes a decrease in Ang II and AT1R, as increase in AT2, ACE2, Ang (1-7) and MasR staining intensity using immunohistochemistry. In addition, the natriuretic effects of tempol were observed in NS-T group, which showed an increased staining intensity of AT2, ACE2, Ang (1-7) and MasR.CONCLUSION:These findings suggest that a high salt diet leads to changes in the homeostasis and balance between opposing components of the renal RAS in hypertension to favour an increase in Ang II. Chronic antioxidant supplementation can modulate the balance between the natriuretic and antinatriuretic components of the renal RAS.Fil: Cao, Gabriel Fernando. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Della Penna, Silvana Lorena. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Kouyoumdzian, Nicolás Martín. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Choi, Marcelo Roberto. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Gorzalczany, Susana Beatriz. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Fernandez, Belisario Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Toblli, Jorge Eduardo. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Roson, Maria Ines. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentin

La alteración de sistemas natriuréticos renales se asocia con el desarrollo de hipertensión arterial y precede en el tiempo a la aparición de daño renal en un modelo de síndrome metabólico

Objetivos: El objetivo del trabajo consistió en determinar la existencia de alteraciones en los sistemas natriuréticos del péptido natriurético atrial y dopamina renal en un modelo de síndrome metabólico por sobrecarga de fructosa y asociarlas con cambios en la presión arterial sistólica, función renal, estado de la Na+, K+-ATPasa y microalbuminuria. Material y Métodos: Ratas macho Sprague-Dawley fueron divididas en grupos control (C) y fructosa (F) con agua o solución de F (10%P/V) para beber durante 4, 8 y 12 semanas. En orina, se midió L-dopa y dopamina, sodio, creatinina y albúmina; y en plasma péptido natriurético atrial, insulina, sodio y creatinina. La presión arterial sistólica fue medida por método indirecto. Se midió la actividad y expresión de la Na+, K+-ATPasa así como la expresión del receptor de péptidos natriuréticos A y C renales. Resultados: La sobrecarga de fructosa se asoció con el aumento de la insulinemia y la presión arterial sistólica, y con la disminución en la excreción urinaria de sodio desde la semana 4. La excreción urinaria de L-dopa se incrementó y la de dopamina disminuyó (cociente L-dopa/dopamina incrementado) por sobrecarga de fructosa desde la semana 4 y el péptido natriurético atrial plasmático se redujo en las semanas 8 y 12. Estos cambios fueron acompañados por un incremento de la actividad y expresión de la Na+, K+- ATPasa, disminución del receptor de péptidos natriuréticos A y aumento del C. La microalbuminuria se observó en la semana 12 de sobrecarga de fructosa.Background: The aim of this study was to determine the presence of alterations in the natriuretic systems of atrial natriuretic peptide and renal dopamine in a model of metabolic syndrome induced by fructose overload and to associate them with changes in systolic blood pressure, renal function, Na+/K+-ATPase status and microalbuminuria. Methods: Male Sprague-Dawley rats were divided into control (C) and fructose (F) groups receiving drinking water or a fructose solution (10% W/V), respectively, for 4, 8 and 12 weeks. L-dopa and dopamine, sodium, creatinine and albumin were measured in urine and ANP, insulin, sodium and creatinine in plasma. Systolic blood pressure was measured by indirect method and the renal activity and expression of Na+/K+-ATPase as well as the renal expression of A- and C-type natriuretic peptide receptors were assessed. Results: Fructose overload was associated with a significant increase in insulinemia and systolic blood pressure levels and a decrease in urinary sodium excretion since week 4. A significant increase in L-dopa excretion and a decrease in dopamine excretion (increased urinary L-dopa/dopamine ratio) due to fructose overload were observed since week 4 with a decrease in plasma atrial natriuretic peptide at weeks 8 and 12. These changes were accompanied by increased activity and expression of Na+/ K+-ATPase, decreased A-type natriuretic peptide receptor and increased C-type natriuretic peptide receptor expression. Microalbuminuria was observed at week 12 of fructose overload. Conclusions: Altered atrial natriuretic peptide and renal dopamine were associated with the development of hypertension and preceded in time the presence of microalbuminuria, thus establishing a temporal association between the alteration of both systems and the development of renal damage.Fil: Rukavina Mikusic, Natalia Lucía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Kouyoumdzian, Nicolás Martín. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: del Mauro, Julieta Sofía. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Farmacología; ArgentinaFil: Gironacci, Mariela Mercedes. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Puyó, Ana María. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Histología y Biología Celular; ArgentinaFil: Toblli, Jorge Eduardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Fernandez, Belisario Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Choi, Marcelo Roberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentin

Consequences of the Lack of IL-10 in Different Endotoxin Effects and its Relationship With Glucocorticoids

Sepsis constitutes one of the major causes of death in ICUs. In sepsis induced by gram-negative, although lipopolysaccharide (LPS) initially induces an exacerbated secretion of proinflammatory cytokines leading to endotoxic shock and death resembling a septic shock, it is also capable of inducing refractoriness to subsequent challenge with LPS, a state known as endotoxin tolerance, which is considered the initial step of the immunosuppression found in septic patients. As we previously demonstrated the importance of glucocorticoids in endotoxin tolerance, the aim of this study was to evaluate the contribution of Interleukin-10 (IL-10) both in the endotoxic shock and in the development of the tolerance and its relationship with glucocorticoids. Our results show that, upon LPS challenge, IL-10 knockout mice (KO) mice had an enhanced LPS sensitivity, along with elevated levels of proinflammatory cytokines as tumor necrosis factor-α, IL-12 and interferon-γ, and enhanced tissue damage, despite the high levels of glucocorticoids. This effect may be because, in part, of the higher expression of tumor necrosis factor receptors in IL-10 KO mice. Further, the injection of dexamethasone did not protect IL-10 KO mice from a LPS lethal challenge. Although tolerance was achieved in the absence of IL-10, it was weaker and the elevated levels of glucocorticoids were not able to reverse the high sensitivity of IL-10 KO mice to LPS. Nevertheless, glucocorticoids would play a pivotal role in the establishment and maintenance of this partial tolerance in IL-10 KO mice. Finally, our results show that IL-10 and glucocorticoids could act in a bidirectional way influencing the inflammatory and anti-inflammatory periods.Fil: Córdoba Moreno, Marlina Olyissa. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Todero, Maria Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Fontanals, Adriana Mirta. Fundación Instituto Leloir; ArgentinaFil: Pineda, Gonzalo Ezequiel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Montagna, Daniela Romina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Yokobori, Noemí. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Ramos, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Barrientos, Gabriela Laura. Hospital Alemán. Laboratorio de Medicina Experimental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Toblli, Jorge Eduardo. Hospital Alemán. Laboratorio de Medicina Experimental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Isturiz, Martín Amadeo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Rearte, María Bárbara. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentin

Left ventricular ejection fraction recovery in patients with heart failure treated with intravenous iron: a pilot study

AimsIn patients with heart failure with reduced ejection fraction (HFrEF) and iron deficiency, treatment with intravenous iron has shown a clinical improvement regardless of anaemic status. Cardiac magnetic resonance (CMR) T2{*} sequence has shown a potential utility for evaluating myocardial iron deficiency. We aimed to evaluate whether T2{*} sequence significantly changes after ferric carboximaltose (FCM) administration, and if such changes correlate with changes in left ventricle ejection fraction (LVEF). Methods and resultsIn this pilot study, we included eight patients with chronic symptomatic (New York Heart Association II-III) HFrEF and iron deficiency. A CMR, including T2{*} analysis, was performed before and at a median of 43days (interquartile range=35-48) after intravenous FCM administration. Pearson or Spearman correlation coefficient (r) was used for bivariate contrast as appropriate. A partial correlation analysis was performed between LVEF and T2{*} while controlling for anaemia status at baseline. Anaemia was present in half of patients. After FCM administration, T2{*} decreased from a median of 39.5 (35.9-48) to 32ms (32-34.5), P=0.012. Simultaneously, a borderline increase in median of LVEF [40\% (36-44.5) to 48.5\% (38.5-53), P=0.091] was registered. In a bivariate correlational analysis, T2{*} was highly correlated with LVEF (r=-0.747, P=0.033). After controlling for anaemia at baseline, the association between T2{*} and LVEF persisted [r(partial): -0.865, R-2(partial): 0.748, P=0.012]. A median regression analysis backed-up these findings. ConclusionsIn a small sample of patients with HFrEF and iron deficiency, myocardial iron repletion assessed by CMR was associated to left ventricular remodelling. Further studies are warranted.S

Beneficial effect of moderate exercise in kidney of rat after chronic consumption of cola drinks

Aim: The purpose of this study was to investigate the effect of moderate intensity exercise on kidney in an animal model of high consumption of cola soft drinks. Methods: Forty-eight Wistar Kyoto rats (age: 16 weeks; weight: 350-400 g) were assigned to the following groups: WR (water runners) drank water and submitted to aerobic exercise; CR (cola runners) drank cola and submitted to aerobic exercise; WS (water sedentary) and CS (cola sedentary), not exercised groups. The aerobic exercise was performed for 5 days per week throughout the study (24 weeks) and the exercise intensity was gradually increased during the first 8 weeks until it reached 20 meters / minute for 30 minutes. Body weight, lipid profile, glycemia, plasma creatinine levels, atherogenic index of plasma (AIP) and systolic blood pressure (SBP) were determined. After 6 months all rats were sacrificed. A kidney histopathological score was obtained using a semiquantitative scale. Glomerular size and glomerulosclerosis were estimated by point-counting. The oxidative stress and proinflammatory status were explored by immunohistochemistry. A one way analysis of variance (ANOVA) with Tukey-Kramer post-hoc test or the Kruskal-Wallis test with Dunn's post-hoc test was used for statistics. A value of p < 0.05 was considered significant. Results: At 6 months, an increased consumption of cola soft drink was shown in CS and CR compared with water consumers (p<0.0001). Chronic cola consumption was associated with increased plasma triglycerides, AIP, heart rate, histopathological score, glomerulosclerosis, oxidative stress and pro-inflammatory status. On the other hand, moderate exercise prevented these findings. No difference was observed in the body weight, SBP, glycemia, cholesterol and plasma creatinine levels across experimental groups. Conclusions: This study warns about the consequences of chronic consumption of cola drinks on lipid metabolism, especially regarding renal health. Additionally, these findings emphasize the protective role of exercise training on renal damage.Fil: Cao, Gabriel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Gonzalez, Julian. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Muller, Maria Angelica. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Ottaviano, Graciela Mabel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Ambrosio, Giuseppe. Università di Perugia; ItaliaFil: Toblli, Jorge Eduardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Milei, Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentin