Plasmodium falciparum parasites grew normally in glutathione (GSH)-depleted normal and G6PD-deficient (Mediterranean variant) erythrocytes (RBC). Growth inhibition was observed only at less than approximately 6-12% residual GSH. Parasites studied separately with the Sendai virus technique synthesized GSH de novo and regenerated reduced GSH 10-20 times faster than non-parasitized RBC. Electron spin resonance measurement of Tempol reduction indicated that the ability to reduce free radicals was restricted to the parasite. The marked efflux of oxidized GSH was mainly derived from the parasite. In conclusion, parasites are endowed with powerful and host-independent mechanisms which de novo synthesize or regenerate GSH and allow undisturbed parasite development in GSH-depleted RBC.

Plasmodium falciparum glutathione metabolism and growth are independent of glutathione system of host erythrocyte.

TURRINI, Francesco Michelangelo;ARESE, Paolo
1998-01-01

Abstract

Plasmodium falciparum parasites grew normally in glutathione (GSH)-depleted normal and G6PD-deficient (Mediterranean variant) erythrocytes (RBC). Growth inhibition was observed only at less than approximately 6-12% residual GSH. Parasites studied separately with the Sendai virus technique synthesized GSH de novo and regenerated reduced GSH 10-20 times faster than non-parasitized RBC. Electron spin resonance measurement of Tempol reduction indicated that the ability to reduce free radicals was restricted to the parasite. The marked efflux of oxidized GSH was mainly derived from the parasite. In conclusion, parasites are endowed with powerful and host-independent mechanisms which de novo synthesize or regenerate GSH and allow undisturbed parasite development in GSH-depleted RBC.
1998
424
257
261
AYI K; CAPPADORO M; BRANCA M; TURRINI F; ARESE P
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/42888
Citazioni
  • ???jsp.display-item.citation.pmc??? 16
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
social impact