Sodium hypochlorite has bactericidal (5000 mg/l, 30 min) and yeasticidal (1000 mg/l, 5 min) activity. Tuberculocidal activity was reported at 1000 mg/l available chlorine in 10 min. The antimicrobial effect of sodium hypochlorite is explained by damage to cellular components and disruption of cell membranes. Cell defence occurs through energy conservation, biofilm formation and the VBNC state. Sodium hypochlorite at 1–5 mg/l mostly increases biofilm mass, whereas 100–5050 mg/l sodium hypochlorite decreases biofilm formation in most species. Moderate removal of biofilm occurs in young biofilms (mostly 21%–87%), less removal is found in mature biofilms. Elevated MIC values indicating tolerance to sodium hypochlorite have been reported in some clinical isolates, but their relevance is uncertain. In bacterial species, there is little or no increase in MIC (≤4-fold) after low-level exposure. Sodium hypochlorite-resistant isolates have been reported for Methylobacterium spp. and R. erythropolis, with insufficient bactericidal activity in suspension tests compared to culture collection strains. No cross-resistance to antibiotics has been reported for S. aureus, but in selected strains of Salmonella spp. Cross-tolerance may be seen to benzalkonium chloride, another quaternary ammonium compound, and alkylamine (L. monocytogenes) or sodium nitrite and hydrogen peroxide (E. coli). The overall probability of resistance to sodium hypochlorite of practical relevance is very low in the absence of biofilm.