Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCA247

Poster Communications

Renal inflammatory response and function in iron overloaded male Wistar rats

A. Ige1, F. Ongele1, E. O. Adewoye1

1. Department of Physiology, University of Ibadan, Ibadan, Oyo, Nigeria.


Iron overload has been recognized to be a risk factor for numerous acute and chronic illnesses likely through increased production of reactive oxygen species (Fashola et al., 2013). Within the kidneys it is likely to cause necrotic renal cells as has been observed to occur in bone marrow cells (Yang et al., 2017). This study investigated renal inflammatory response and function in iron-overloaded male Wistar rats. Thirty-animals were equally distributed into 3 groups and treated with either normal saline (0.2ml; control), iron (as ferrous sulphate) at 15mg/kg and iron at 30mg/kg for 21 days respectively. All treatment was daily administered intraperitoneally. At 21-days post-treatment, blood samples were obtained by cardiac puncture after light intraperitoneal sodium thiopenthal anesthesia into plain sample bottles. Serum was obtained from these samples and analyzed for iron, ferritin, transferrin, creatinine, urea, albumin, total protein, interleukin-6 (IL-6), prostaglandins E-2 (PGE-2), and tumor necrotic factor-a (TNF-a). Kidney homogenates were also obtained from 5 animals in each group and analysed for superoxide dismutase (SOD), total antioxidant capacity (TAC), reduced glutathione (GSH), lipid peroxidation (MDA) and nitric oxide levels. Kidney samples were obtained from the remaining 5 animals in each and analysed using H and E and periodic acid Schiff stains. Results are presented as Data were expressed as Mean±SEM and statistical significance was taken at p<0.05 using the Student's T-test. Graded increase (p<0.05) in serum iron (mg/dL)(84.6±14.4; 90.5±5.5 vs. 58.8±2.1), ferritin (mg/dL)(27.5±5.9; 58.6±5.7 vs. 11.4±1.7), transferrin (mg/dL)(149.4±14.6; 163.3±4.9 vs 64.8±6.6), creatinine (mmol/L)(243.4±33.2; 163.2±14.3 vs. 120.1±18.5), urea (mg/dl)(1.03±0.01; 1.37±0.01 vs. 0.81±0.19), IL-6 (pg/ml)(14.7±1.2; 19.5±3.7), TNF-a (pg/ml)(17.5±1.7; 25.6±1.4 vs. 6.4±1.1) and a reduction (p<0.05) in albumin (g/dL)(2.09±0.02; 1.64±0.16 vs. 3.08±0.03) levels were observed in groups 2 (iron 15mg/kg) and 3 (Iron 30mg/kg) respectively compared to control. Graded reductions in renal SOD (U/ml)(0.16±0.01; 0.12±0.01 vs. 0.34±0.02), GSH (mM) (0.11±0.04; 0.017±0.02 vs. 0.25±0.03) and increases in TAC (mM)(0.81±0.26; 1.86±0.51 vs. 0.23±0.12), MDA (mM)(0.53±0.03; 0.60±0.01 vs. 0.26±0.04) and nitric oxide (mM) (30.7±3.1; 31.4±2.6 vs. 10.2±1.7) levels were observed in groups 2 and 3 compared to control. Histological evaluation of the kidney showed structural and tubular aberrations consistent with renal damage via inflammatory processes in groups 2 and 3 compared to control. The data obtained from this study suggests that iron-overload causes renal dysfunction by triggering a cascade of systemic and renal inflammatory processes, which then alters renal structure and function.

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