## 1 Introduction  
The discovery of antibiotics raised hope that a powerful tool to control harmful and pathogenic microorganisms has been found. Unfortunately, extensive research has revealed that the fight against microbes remains a constant challenge. For this reason, the development of new drugs with enhanced antibacterial potencies is still needed ([1; 2; 3], and refs. therein). Amid the most plausible, fast and cost-efficient approaches, drugs developed for the treatment of other diseases are also increasingly utilized. Hence, in this context, the testing of drugs used for cancer therapy is becoming a common issue ([2; 3; 4; 5], and refs. therein). Cancer and bacterial cells have many properties in common, such as a high replication rate, virulence, ways of spreading within the host, rapid development of resistance mechanisms and a tendency to become more aggressive during disease progression, which implies that some anticancer drugs may act as efficient antibacterial agents, and _vice versa_[2; 6; 7; 8]. Heterocyclic di-N-oxides (HNOXs) have garnered special attention due to their antitumor as well as antiviral and antimicrobial activities ([9; 10; 11; 12; 13; 14], and refs. therein). Among them, quinoxaline (benzopyrazine or benzodiazep) di-N-oxides (QDNOXs) such as carbodox, olaquindox, mequindox, cyadox, quinocetone etc. were found to be efficient agents against many Gram-positive and -negative bacterial strains ([12; 13; 14; 15; 16], and refs. therein). The \(N\)-oxide moiety of HNOXs with the highest local electrophilic potency is considered to be a key functional (electron-accepting) group governing the redox conversion of these compounds. In this case, the enzymatic (or non-enzymatic) reduction of HNOXs to their free radical intermediates is rapidly accompanied by the generation of reactive oxygen species (ROS) ([12; 13], and refs. therein). Recently performed transcriptomic and proteomic studies of _E. coli_ strains have provided clear evidence that HNOXs induce ROS generation accompanied by DNA cleavage, involving a substantial contribution of putative reductases in bacteria [12; 13]. In general, ROS generation involves a multi-targeting damaging process, in contrast to that of the most antibiotics, which act specifically to a definite target. Amongst the HNOXs, 3-amino-1,2,4-benzotriazine-1,4-dioxide (tirapazamine (TPZ), SR4233 or WIN 59075) is one of the most prominent anticancer drugs, which underwent phase 2-3 clinical trials and subsequent studies involving liver chemo-embolization. Greater pre-clinical and clinical treatment outcomes were achieved when TPZ was used in combination with other chemotherapeutic agents ([4; 17; 18], and refs. therein). TPZ has been shown to be an excellent electron-accepting substrate of extracellular reductases (e.g., NAD(P)H-dependent flavoenzymes such as cytochrome P-450 reductase (P-450R), ubiquinone reductase (complex I), nitric oxide synthase (NOS), etc. ), reducing a pro-drug to its radical intermediate, accompanied by ROS generation causing DNA damage, chromosome aberration and other events ([13; 19; 20; 21; 22], and refs. therein). In addition to its antitumor activity, triapazamine has been found to be an efficient antifungal and antibacterial agent with respect to Gram-negative and -positive bacterial strains such as _Escherichia coli_ and _Staphylococcus aureus_, respectively, as well as various _Clostridium difficile_ strains [4]; antibiotic resistant _E. coli_ and _S. aureus_ showed virtually the same susceptibility to this drug as wild type strains. Further studies revealed that _E. coli_ mutants carrying deletions of genes involved in DNA repair were highly susceptible to TPZ, while those with deleted genes encoding putative reductases showed resistance to TPZ, which suggested that the inhibitory potency of this drug is likely to be caused by its reductive activation by bacterial reductases [4]. Since TPZ functions primarily as a hypoxia selective cytotoxin ([4; 11; 13; 18; 22], and refs.