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. Author manuscript; available in PMC: 2020 Nov 23.
Published in final edited form as: Biochem Pharmacol. 2019 Aug 14;169:113604. doi: 10.1016/j.bcp.2019.08.006

Figure 11. Downregulation of CSE influences porphyrin and heme synthesis.

Figure 11.

Ablation of H2S biosynthesis in the CSE−/− mice or pharmacological inhibition of CSE activity in liver cells yields: (1) elevated red blood cell counts, red blood cell MCVs, hematocrit, hemoglobin and heme levels in plasma samples of CSE−/− mice; (2) reduced CSE-derived H2S production, increased heme level, CPOX protein expression and mitochondrial function in liver samples of CSE−/− mice; (3) pharmacological inhibition of CSE activity in liver cell cultures increases CPOX gene promoter activity whereas addition of H2S suppresses it; (4) elevated uroporphyrinogen III and reduced coproporphyrinogen III can be detected in the urine samples of CSE−/− mice, suggestive of increased CPOX enzyme activity. RBC: red blood cell; MCV: mean corpuscular volume; Ht: hematocrit; Hb: hemoglobin; CPOX: Coproporphyrinogen oxidase; PpIX: Protoporphyrin IX.