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Sunlight inhibits growth and induces markers of programmed cell death in Plasmodium falciparum in vitro.

Engelbrecht D, Coetzer TL - Malar. J. (2015)

Bottom Line: Mitochondrial hyperpolarization likely resulted from increased oxidative stress.Although data suggested increased phosphatidylserine externalization in mixed-stage parasites, results were not statistically significant.The combination of biochemical markers and the survival of some parasites, despite exposure to a lethal stimulus, support the occurrence of PCD in P. falciparum.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Medicine and Haematology, Faculty of Health Sciences, School of Pathology, Wits Medical School, Wits Research Institute for Malaria, University of the Witwatersrand, 7th floor, 7 York Road, Parktown, Johannesburg, 2193, South Africa. dewaldtengelbrecht@gmail.com.

ABSTRACT

Background: Plasmodium falciparum is responsible for the majority of global malaria deaths. During the pathogenic blood stages of infection, a rapid increase in parasitaemia threatens the survival of the host before transmission of slow-maturing sexual parasites to the mosquito vector to continue the life cycle. Programmed cell death (PCD) may provide the parasite with the means to control its burden on the host and thereby ensure its own survival. Various environmental stress factors encountered during malaria may induce PCD in P. falciparum. This study is the first to characterize parasite cell death in response to natural sunlight.

Methods: The 3D7 strain of P. falciparum was cultured in vitro in donor erythrocytes. Synchronized and mixed-stage parasitized cultures were exposed to sunlight for 1 h and compared to cultures maintained in the dark, 24 h later. Mixed-stage parasites were also subjected to a second one-hour exposure at 24 h and assessed at 48 h. Parasitaemia was measured daily by flow cytometry. Biochemical markers of cell death were assessed, including DNA fragmentation, mitochondrial membrane polarization and phosphatidylserine externalization.

Results: Sunlight inhibited P. falciparum growth in vitro. Late-stage parasites were more severely affected than early stages. However, some late-stage parasites survived exposure to sunlight to form new rings 24 h later, as would be expected during PCD whereby only a portion of the population dies. DNA fragmentation was observed at 24 and 48 h and preceded mitochondrial hyperpolarization in mixed-stage parasites at 48 h. Mitochondrial hyperpolarization likely resulted from increased oxidative stress. Although data suggested increased phosphatidylserine externalization in mixed-stage parasites, results were not statistically significant.

Conclusion: The combination of biochemical markers and the survival of some parasites, despite exposure to a lethal stimulus, support the occurrence of PCD in P. falciparum.

No MeSH data available.


Related in: MedlinePlus

No significant change was seen in the phosphatidylserine externalization of parasitized erythrocytes after exposure sunlight. Flow cytometry histograms (upper panels) showed an apparent increase in PS externalization in mixed-stage pRBC at both 24 (a) and 48 (c) hours after one and two exposures to sunlight, respectively. However, statistical analyses of bar graphs (bottom panels) showed no significant differences (ns). Synchronized late-stage pRBC exposed to solar radiation for 1 h and maintained in the dark for the remainder of 24 h also showed no change in PS externalization, compared to control cultures maintained in the dark (b). n = 2 for (a) and (b); n = 4 for (c)
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Fig5: No significant change was seen in the phosphatidylserine externalization of parasitized erythrocytes after exposure sunlight. Flow cytometry histograms (upper panels) showed an apparent increase in PS externalization in mixed-stage pRBC at both 24 (a) and 48 (c) hours after one and two exposures to sunlight, respectively. However, statistical analyses of bar graphs (bottom panels) showed no significant differences (ns). Synchronized late-stage pRBC exposed to solar radiation for 1 h and maintained in the dark for the remainder of 24 h also showed no change in PS externalization, compared to control cultures maintained in the dark (b). n = 2 for (a) and (b); n = 4 for (c)

Mentions: Flow cytometry data showed increased PS externalization in mixed-stage pRBC on the day following both the first (Fig. 5a) and second exposure (Fig. 5c) to natural sunlight, but the difference was not statistically significant. No increase in PS externalization was observed in synchronized late-stage pRBC exposed to sunlight (Fig. 5b).Fig. 5


Sunlight inhibits growth and induces markers of programmed cell death in Plasmodium falciparum in vitro.

Engelbrecht D, Coetzer TL - Malar. J. (2015)

No significant change was seen in the phosphatidylserine externalization of parasitized erythrocytes after exposure sunlight. Flow cytometry histograms (upper panels) showed an apparent increase in PS externalization in mixed-stage pRBC at both 24 (a) and 48 (c) hours after one and two exposures to sunlight, respectively. However, statistical analyses of bar graphs (bottom panels) showed no significant differences (ns). Synchronized late-stage pRBC exposed to solar radiation for 1 h and maintained in the dark for the remainder of 24 h also showed no change in PS externalization, compared to control cultures maintained in the dark (b). n = 2 for (a) and (b); n = 4 for (c)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4588498&req=5

Fig5: No significant change was seen in the phosphatidylserine externalization of parasitized erythrocytes after exposure sunlight. Flow cytometry histograms (upper panels) showed an apparent increase in PS externalization in mixed-stage pRBC at both 24 (a) and 48 (c) hours after one and two exposures to sunlight, respectively. However, statistical analyses of bar graphs (bottom panels) showed no significant differences (ns). Synchronized late-stage pRBC exposed to solar radiation for 1 h and maintained in the dark for the remainder of 24 h also showed no change in PS externalization, compared to control cultures maintained in the dark (b). n = 2 for (a) and (b); n = 4 for (c)
Mentions: Flow cytometry data showed increased PS externalization in mixed-stage pRBC on the day following both the first (Fig. 5a) and second exposure (Fig. 5c) to natural sunlight, but the difference was not statistically significant. No increase in PS externalization was observed in synchronized late-stage pRBC exposed to sunlight (Fig. 5b).Fig. 5

Bottom Line: Mitochondrial hyperpolarization likely resulted from increased oxidative stress.Although data suggested increased phosphatidylserine externalization in mixed-stage parasites, results were not statistically significant.The combination of biochemical markers and the survival of some parasites, despite exposure to a lethal stimulus, support the occurrence of PCD in P. falciparum.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Medicine and Haematology, Faculty of Health Sciences, School of Pathology, Wits Medical School, Wits Research Institute for Malaria, University of the Witwatersrand, 7th floor, 7 York Road, Parktown, Johannesburg, 2193, South Africa. dewaldtengelbrecht@gmail.com.

ABSTRACT

Background: Plasmodium falciparum is responsible for the majority of global malaria deaths. During the pathogenic blood stages of infection, a rapid increase in parasitaemia threatens the survival of the host before transmission of slow-maturing sexual parasites to the mosquito vector to continue the life cycle. Programmed cell death (PCD) may provide the parasite with the means to control its burden on the host and thereby ensure its own survival. Various environmental stress factors encountered during malaria may induce PCD in P. falciparum. This study is the first to characterize parasite cell death in response to natural sunlight.

Methods: The 3D7 strain of P. falciparum was cultured in vitro in donor erythrocytes. Synchronized and mixed-stage parasitized cultures were exposed to sunlight for 1 h and compared to cultures maintained in the dark, 24 h later. Mixed-stage parasites were also subjected to a second one-hour exposure at 24 h and assessed at 48 h. Parasitaemia was measured daily by flow cytometry. Biochemical markers of cell death were assessed, including DNA fragmentation, mitochondrial membrane polarization and phosphatidylserine externalization.

Results: Sunlight inhibited P. falciparum growth in vitro. Late-stage parasites were more severely affected than early stages. However, some late-stage parasites survived exposure to sunlight to form new rings 24 h later, as would be expected during PCD whereby only a portion of the population dies. DNA fragmentation was observed at 24 and 48 h and preceded mitochondrial hyperpolarization in mixed-stage parasites at 48 h. Mitochondrial hyperpolarization likely resulted from increased oxidative stress. Although data suggested increased phosphatidylserine externalization in mixed-stage parasites, results were not statistically significant.

Conclusion: The combination of biochemical markers and the survival of some parasites, despite exposure to a lethal stimulus, support the occurrence of PCD in P. falciparum.

No MeSH data available.


Related in: MedlinePlus