*3.6. Renal Mitochondrial Function*

Uraemic animals demonstrated that in renal tissue mitochondria, there was a significant increase in inefficiency (enhanced proton leak and complex I dysfunction) (Figure 8a). Iron therapy produced a mixed and complex result with no change in the protein leak but an increased maximal respiration and respiratory reserve capacity suggesting improved mitochondrial oxidative capacity. However, there was a reduction of complex II and complex IV driven respiration (Figure 8b), which would sugges<sup>t</sup> a degree of mitochondrial dysfunction.

**Figure 8.** Isolated Mitochondrial measures of function including Respiratory rates and mitochondrial respiration in the presence of: (**A**) 0.5 μg mitochondrial protein, 10 mM succinate and 2 μM rotenone; (**B**) 0.6g mitochondrial protein, 10 mM pyruvate, 2 mM malate and 4 μM FCCP (carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone) with or without 10 mM malonate. In Fig 8B the electron transport chains complexes I, II and IV were measured. Results are presented as mean ± SEM. (\* *p* < 0.05; \*\* *p* < 0.01). Proton leak = (minimum rate measured after Oligomycin injection) − (non-mitochondrial respiration rate or minimum rate measured after injection of Antimycin A); Maximal respiration = (maximal rate measured after FCCP injection) – (non-mitochondrial respiration rate); Respiratory reserve capacity = (maximal respiration – basal respiration).
