Manganese superoxide dismutases (MnSODs) play a pivotal role in the preservation of mitochondrial integrity and function in fungi under various endogenous and exogenous stresses. Deletion of Aspergillus nidulans mnSOD/sodB increased oxidative stress sensitivity and apoptotic cell death rates as well as affected antioxidant enzyme and sterigmatocystin productions, respiration, conidiation and the stress tolerance of conidiospores. The physiological consequences of the lack of sodB were more pronounced during carbon-starvation than in the presence of glucose. Lack of SodB also affected the changes in the transcriptome, recorded by high-throughput RNA sequencing, in menadione sodium bisulfite (MSB)-exposed, submerged cultures supplemented with glucose. Surprisingly, the difference between the global transcriptional changes of the ?sodB mutant and the control strain was relatively small indicating that the SodB-dependent maintenance of mitochondrial integrity was not essential under these experimental conditions. Owing to the outstanding physiological flexibility of the Aspergilli, certain antioxidant enzymes and endogenous antioxidants together with the reduction in mitochondrial functions well compensated for the lack of SodB. The lack of sodB reduced the growth of surface cultures more than submerged culture, which should be considered in future development of fungal disinfection methods. Overall design: Comparative gene expression profiling analysis of RNA-seq data for mycelia of Aspergillus nidulans reference strain, and DsodB mutant under menadione (MSB) treated and untreated conditions with three biological replicates.