Carbonic anhydrase (CA) is a ubiquitous metalloenzyme involved in a number of physiological processes including respiration, pH homeostasis, electrolyte transport, calcification, biosynthetic reactions. The aim of this work was to explore a novel functional role of CA in animals: its involvement in the lysosomal system response to metal exposure. Mytilus galloprovincialis digestive gland was used as experimental model. The in vivo exposure of mussels to CdCl2 was able to evoke the induction of digestive gland CA. This response was paralleled by the activation of the lysosomal compartment (proliferation and/or increase in size of lysosomes), as assessed on LysoSensor Green marked cells by confocal microscopy and spectrofluorimetric analysis. When mussels were in vivo exposed to acetazolamide, specific CA inhibitor, the acidification of the lysosomal compartment was prevented. Moreover, during the co-exposure to cadmium and acetazolamide, the cadmium induced activation of the lysosomal compartment was completely inhibited. In conclusion, our results demonstrated in vivo the physiological contribution of CA to the acidification of the lysosomal compartment in digestive gland and its involvement in the lysosomal activation following cadmium exposure. CA induction following cadmium exposure could physiologically sustain a prolonged increased requirement of H+ for supporting lysosomal acidification during lysosomal activation.
A novel physiological role for carbonic anhydrase in animals: involvement in the lysosomal response to cadmium exposure in mussel digestive gland
Caricato Roberto;Giordano Maria Elena;Schettino Trifone;Lionetto Maria Giulia
2018-01-01
Abstract
Carbonic anhydrase (CA) is a ubiquitous metalloenzyme involved in a number of physiological processes including respiration, pH homeostasis, electrolyte transport, calcification, biosynthetic reactions. The aim of this work was to explore a novel functional role of CA in animals: its involvement in the lysosomal system response to metal exposure. Mytilus galloprovincialis digestive gland was used as experimental model. The in vivo exposure of mussels to CdCl2 was able to evoke the induction of digestive gland CA. This response was paralleled by the activation of the lysosomal compartment (proliferation and/or increase in size of lysosomes), as assessed on LysoSensor Green marked cells by confocal microscopy and spectrofluorimetric analysis. When mussels were in vivo exposed to acetazolamide, specific CA inhibitor, the acidification of the lysosomal compartment was prevented. Moreover, during the co-exposure to cadmium and acetazolamide, the cadmium induced activation of the lysosomal compartment was completely inhibited. In conclusion, our results demonstrated in vivo the physiological contribution of CA to the acidification of the lysosomal compartment in digestive gland and its involvement in the lysosomal activation following cadmium exposure. CA induction following cadmium exposure could physiologically sustain a prolonged increased requirement of H+ for supporting lysosomal acidification during lysosomal activation.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.