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. Author manuscript; available in PMC: 2014 Oct 1.
Published in final edited form as: Neurobiol Aging. 2013 Apr 17;34(10):2322–2330. doi: 10.1016/j.neurobiolaging.2013.03.024

Fig. 4.

Fig. 4

Neuronal expression of zinc-deficient SOD (CuSOD) sensitizes flies to zinc and paraquat toxicity. (A) Neuronal expression of zinc-deficient superoxide dismutase (SOD1 or CuSOD) leads to a decrease in ATP levels of fly heads (p=0.005). (B) and (C) Neuronal expression of CuSOD sensitizes flies to paraquat toxicity, whereas expression of wild-type human SOD1 (hSOD1) enhances resistance to paraquat (p<0.0001). (D) Neuronal expression of CuSOD sensitizes larvae to zinc (p=0.003) but not iron or copper toxicity (p>0.05). Relative survival represents eclosion ratio of females (Elav-GAL4/+ for control, Elav-GAL4/UAS-D83S for CuSOD, Elav-GAL4/UAS-hSOD1 for hSOD1) to male files (+/+ for control, +/UAS-D83S for CuSOD, +/UAS-hSOD1 for hSOD1) on different media. (E) Expression of hSOD1 does not sensitize flies to zinc toxicity. Genotypes were as follows: control (Elav-GAL4/+), hSOD1 (Elav-GAL4/UAS-hSOD1), CuSOD1 (Elav-GAL4/UAS-D83S1), CuSOD or CuSOD2 (Elav-GAL4/UAS-D83S2). For panels (A), (D), and (E), the significance of the difference between means was analyzed using 1-way analysis of variance. For (B) and (C), the significance of the difference between survival curves was analyzed using log-rank test.