Previous studies revealed a close connection between heat shock and manganese-dependent superoxide dismutase (SOD2) in eukaryotes. This paper shows that SOD mimics based on manganese complexes caused an increase in thermotolerance for a mutant fission yeast deficient in mitochondrial superoxide dismutase. Manganese compounds used for tests are SOD mimics, from two different classes: salen manganese (EUK-8) and Mn porphyrin (MnIIITE-2-PyP5+). The tests were conducted using a Schizosaccharomyces pombe model, comparing the viability of two strains at chronic heat stress (37°C)—a wild type versus a strain with the mitochondrial superoxide dismutase gene deleted [SOD2(−)]. The presence of massive free radical species in S. pombe SOD2(−) was demonstrated using a luminol-enhanced chemiluminescence test derived from a menadione-mediated survival protocol. Conclusions: Survival tests revealed that the SOD2-deleted S. pombe is about 100 times more sensitive to heat stress than the wild-type strain. This survival deficit can be corrected by EUK-8 and MnIIITE-2-PyP5+ to almost the same degree but not by manganese chloride II (MnCl2). Using a simple spot assay for viability testing, this new model proved to be an easy alternative for the initial estimation of manganese SOD mimics efficiency.