Effect of thioglycolic acid molecules on luminescence properties of $$\hbox {Ag}_2$$S quantum dots

For monoclinic $$\hbox {Ag}_2$$S nanocrystals (quantum dots, $$\hbox {Ag}_2$$S/TGA QDs), the correlation between their luminescence properties and aspects of their passivation by thioglycolic acid (TGA) molecules is considered. The features of quantum confinement effect in the QDs absorption and photoluminescence spectra are analyzed for $$\hbox {Ag}_2$$S QDs with an average size of 1.7–3.1 nm. We show that, in various conditions of passivation of QDs interfaces, the luminescence mechanism of $$\hbox {Ag}_2$$S/TGA QDs is switched from recombination luminescence in the 870–1000 nm region to exciton luminescence with a band maximum at 620 nm. By means of FTIR spectra, two major types of interactions between TGA molecules and $$\hbox {Ag}_2$$S QDs, arising due to changing the [$$\hbox {Ag}^+$$]:[$$\hbox {S}^{2-}$$] ratio from 1:0.9 to 1:1.43, are determined. Exciton luminescence (620 nm) occurs in case of using TGA as the sulfur source in $$\hbox {Ag}_2$$S crystallization and the interface passivation agent, with [$$\hbox {Ag}^+$$]:[$$\hbox {S}^{2-}$$] = 1:1. The analysis of the FTIR spectra indicates bonding of TGA with the $$\hbox {Ag}_2$$S surface by both thiol and carboxylic groups in this case. With increasing the sulfur concentration in the synthesis of $$\hbox {Ag}_2$$S/TGA QDs, the exciton luminescence is suppressed. The employment of $$\hbox {Na}_2$$S as the sulfur source in $$\hbox {Ag}_2$$S crystallization with TGA acting as the surface passivation agent promotes the formation of recombination centers for IR luminescence. In this case, analysis of the FTIR spectra indicates passivation of $$\hbox {Ag}_2$$S QDs by TGA molecules due to adsorption of thiol groups. It is found that the photodegradation or IR luminescence of $$\hbox {Ag}_2$$S/TGA QDs upon exposure to exciting radiation is due to the photolysis of $$\hbox {Ag}_2$$S nanocrystals with formation of luminescence quenching centers as well as due to photodestruction of TGA molecules.