Fig. 4: Sp prevents oxidative cellular and mitochondrial damage.
a, b Eye imaginal disks derived from wild type or park13 third instar larvae, stained with anti-elav antibody to label the rhabdomeres and imaged with confocal microscope. Scale bar: 30 µm. The number of rhabdomeres was counted and represented as mean ± s.e.m.; n = 3, *P (t-test) <0.01 (b). c The extent of lipid peroxidation in 2.5 mM Sp treated/untreated wild type or mutant brains was measured by quantifying the levels of malondialdehyde (MDA) through thiobarbituric acid reactive substances assay. d The respiratory complex I activity was measured by observing the decrease in absorbance at 340 nm due to oxidation of NADH. Bars represent mean ± s.e.m.; n = 3, **P (t-test) <0.001. e The maintenance of mitochondrial membrane potential in park13 flies was measured by retention of TMRE dye in neuronal mitochondria and represented as fold change over untreated wild type. f The accumulation of mitochondrial mass in neurons of fly brain due to Sp treatment was determined by measuring the relative uptake N-Nonyl Acridine Orange (NAO) dye over the untreated samples. g The levels of mitochondrial superoxides in respective fly brains were estimated through quantification of MitoSOX fluorescence intensity (FI) and denoted as fold change over untreated wild type. All data are represented as mean ± s.e.m.; n = 10, **P (t-test) <0.001, *P (t-test) < 0.01.
