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. 2020 Jan 16;11:4. doi: 10.1186/s13293-019-0280-4

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© The Author(s). 2020

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 7 — Cyp1b1 gene disruption minimized angiotensin (Ang II)-induced superoxide production, which was reversed by 6β-hydroxytestosterone (6β-OHT). Cyp1b1^+/+ and Cyp1b1^−/− mice were infused with vehicle or Ang II (700 ng/kg/day) (upper panel) and treated with 6β-OHT (15 μg/g b.w every third day) or 6β-OHT+Ang II (lower panel) for 14 days. Aortic superoxide production was determined by the fluorescence intensity of 2-hydoxyethidium (a, b). Photomicrographs are representative of the aorta from mice in each of the different treatment groups following incubation with dihydroethidium. The graph depicts the quantified data. *P < 0.05 vehicle, 6β-OHT vs. corresponding value from Ang II-treated animal; ^†P < 0.05 Cyp1b1^+/+ Ang II vs. Cyp1b1^−/− Ang II (n = 3 for all experiments, unpaired t test; data are expressed as mean ± SEM)