Figure 5

Proposed mechanism of biomimetic CdTe-GSH QDs toxicity in E. coli . Upon QDs exposure membrane damage is produced (1) with the concomitant generation of an envelope stress (1a). Furthermore, QDs are able to release metal/metalloid ions from the nanoparticle core, such as Cd²⁺ and Te²-(2). Since telluride (Te²-) present in CdTe QDs is easily oxidized into insoluble Te⁰, its contribution to QD toxicity is minor (3). Cadmium is released from the nanoparticle and enters the cell by divalent metal transporters (4). Once inside, metal affinity for reduced thiol groups produces RSH depletion (5). When the pool of oxidized thiols increase, the cell undergoes oxidative stress (6), which will increase ROS generation, resulting in protein damage and Fe²⁺ release (6b). All these processes generate a major transcriptional response associated with cadmium (7) and its secondary effects related with oxidative stress (8) and metabolic reconfiguration (9). Moreover, bacteria modulates the influx and efflux of toxic metals (10 a,b), promoting the exit of cadmium from the cell (zntA) and the entry of antioxidant molecules like Zn²⁺ (znuA) (10c). On the other hand, CdTe-GSH seem to elicit a QDs response mediated by ybgK, clpS, hylC, yfcF, nrfC, among others, which involves genes different from those modulated in response to cadmium stress (11). The ybgK gene is strongly up-regulated after both QDs treatment and has no known function.