# Microbial-Based Biotechnology: Production and Evaluation of Selenium-Tellurium Nanoalloys
## 4 Discussion
The CdTe QDs had excellent crystallinity and consistent size. It was less toxic to eukaryotic cells when compared to hydrothermally synthesized particles. CdTe QDs can be used for cancer treatments due to their low toxicity [34]. Nanoparticle formation is usually considered as a defense mechanism against metal toxicity. The enhanced excretion or reduced absorption of the metals is their primary response to exposure to high metal concentrations. It includes either reductive precipitation or volatilization of selenite/tellurite [42; 43]. A low degree of innate susceptibility to SeO\({}_{3}\)\({}^{2-}\)/TeO\({}_{3}\)\({}^{2-}\) was exhibited by certain Gram-positive and Gram-negative bacteria [44; 45]. Tellurite resistance has been established to be caused by chromosomal (Te\({}^{\text{R}}\)) and plasmid-mediated tellurite resistance (Te\({}^{\text{R}}\)) determinants [44]. Several enzymatic reductions by bacteria have been reported, such as thiol or glutathione reductase [46; 47], sulphite reductase [48], fumarate reductase [49; 50], Painter-type reaction [51], and nitrite reductase [52; 53; 54]. Depending on the bacterial type, the enzymatic reduction reaction can happen in the cytoplasm or periplasm [54]. [PERSON] et al. [55] explain that the TeO\({}_{3}\)\({}^{2-}\) enters the cell via the phosphate transporter. Nitrate reductases reduce it [52], where TeO\({}_{3}\)\({}^{2-}\) can be reduced to Te\({}^{0}\). It can also be enzymatically converted to volatile hydride or methyl compounds via cellular-reduced thiols. Once selenite/tellurite enters the periplasm, it cannot be used as a distinctive electron acceptor. Reductase enzymes can reduce into Se\({}^{0}\)/Te\({}^{0}\)/SeTe-NAs [56]. Figure 6 explains the extracellular and intracellular formation of selenium. In the cytoplasm, Se\({}^{0}\)/Te\({}^{0}\)/SeTe-NAs formations are followed by the assembly of Se nanospheres/Te nanorods/SeTe-NAs poly-amorphous structures. Intracellular transport mechanisms are exhibited by cells to prevent accumulations of Se nanospheres/Te nanorods/SeTe-NAs [38; 57]. _T. selenatis_ transports the Se nanospheres out of the cell from the cytoplasm. Selenite is reduced to Se\({}^{0}\) followed by the binding of Se\({}^{0}\) protein for assembling the Se nanosphere. It is lysed or transported outside the cell by an unknown mechanism [58; 59]. Many unspecific proteins only interact with intracellular Se-NPs, resulting in excellent colloidal stability [60]. There is also an extracellular synthesis in the cytoplasm where selenite/tellurite is reduced to Se\({}^{0}\)/Te\({}^{0}\)/SeTe-Nas (Figure 7). It is followed by transportation across the membrane as a foreign entity outside the cell by an unknown export mechanism. Then, Se\({}^{0}\)/Te\({}^{0}\)/SeTe-NAs nuclei are assembled outside the cell into Se nanospheres/Te nanorods/SeTe-NAs poly-amorphous structures through an Ostwald-type ripening mechanism [39; 40]. A similar possible mechanism has been reported by [PERSON] et al. in silver nanoparticle synthesis [61]. Day by day, more concern is given to the green synthesis of Se- and Te-NPs, as reported by [PERSON] et al. [62].