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J Comp Pathol 1992 Apr;106(3):213-20
Immunohistochemical identification of ferritin, lactoferrin and transferrin in
leprosy lesions of human skin biopsies.
Momotani E, Wuscher N, Ravisse P, Rastogi N
Unite de la Tuberculose et des Mycobacteries, Institut Pasteur, Paris,
France.
Granulomatous lesions of human leprosy contained ferritin and
lactoferrin but little or no transferrin, as demonstrated by the
avidin-biotin complex immunoperoxidase method. Lactoferrin was found
in the neutrophils. These results suggested that the cells of the host
mononuclear phagocyte system in leprosy granulomas provide an adequate
nutritional environment for iron acquisition by M. leprae. A possible
role of iron binding proteins in the granulomas is discussed in
relation to previous data on bovine paratuberculous granulomas.
PMID: 1602055, UI: 92291380
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Pharm Weekbl Sci 1989 Feb 24;11(1):3-8
Pharmacochemical aspects of leprosy. Recent developments and prospects for new
drugs.
van Saane P, Timmerman H
Division of Pharmacochemistry, Free University, Amsterdam, The
Netherlands.
From a pharmacochemical point of view the existing anti-leprotics as
well as possible innovations in the chemotherapy of leprosy are
discussed. Of the main anti-leprotics, which are used
nowadays--dapsone, rifampicin, clofazimine, isoniazide, ethionamide
and prothionamide--the mechanism of action, the main problems in their
application and possibilities to develop improved variants are
reviewed. Based on the chemistry of Mycobacterium leprae, the target
systems for new anti-leprotics are identified. These systems include
the cell wall, the catabolism of reactive oxygen species, the
metabolisms of carbon sources, the amino acid metabolism and the
uptake of iron. Two possible new lead structures from other fields,
4-quinolones and mycobacterial ribonucleotide reductase inhibitors are
presented.
Publication Types:
* Review
* Review, tutorial
PMID: 2652092, UI: 89220374
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J Antimicrob Chemother 1995 Jan;35(1):23-9
Effect of iron chelation on the in-vitro growth of Leishmania promastigotes.
Soteriadou K, Papavassiliou P, Voyiatzaki C, Boelaert J
Laboratory of Biochemistry, Hellenic Pasteur Institute, Athens,
Greece.
The development of vaccines and drugs to control leishmaniasis is
urgently needed. The presence of a leishmania transferrin receptor on
the parasite suggests that an adequate supply of iron is needed for
the life cycle of leishmania. We have investigated the effect of iron
deprivation on the growth of leishmania promastigotes in vitro using
an iron chelation approach. All chelators tested reduced the rate of
promastigote multiplication in a dose-dependent fashion, whereas
referrated ones did not. The hydroxypyridin-4-one chelators CP94 and
L1 were found to be more efficient than desferrioxamine. We suggest
that iron depletion may be an effective mechanism against leishmania
infection.
PMID: 7768775, UI: 95286457
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Infect Immun 1994 Aug;62(8):3262-9
Acquisition of iron from transferrin and lactoferrin by the protozoan
Leishmania chagasi.
Wilson ME, Vorhies RW, Andersen KA, Britigan BE
Department of Internal Medicine, University of Iowa College of
Medicine, Iowa City.
Leishmania chagasi, the cause of South American visceral
leishmaniasis, requires iron for its growth. However, the extent to
which different iron sources can be utilized by the parasite is not
known. To address this question, we studied acquisition of iron from
lactoferrin and transferrin by the extracellular promastigote form of
L. chagasi during growth in vitro. A promastigote growth medium based
on minimal essential medium supplemented with iron-depleted serum
supported promastigote growth only after the addition of exogenous
iron. The addition of 8 microM iron chelated to lactoferrin or hemin
resulted in normal promastigote growth. Ferritransferrin also
supported promastigote growth, but only after a considerable lag.
Promastigotes grown in all three iron sources generated similar
amounts of hydroxyl radical upon exposure to hydrogen peroxide,
indicating that none of these protected parasites against generation
of this toxic radical. Promastigotes were able to take up 59Fe
chelated to either transferrin or lactoferrin, although uptake from
59Fe-lactoferrin occurred more rapidly. 59Fe uptake from either
59Fe-transferrin or 59Fe-lactoferrin was inhibited by a 10-fold excess
of unlabeled ferrilactoferrin, ferritransferrin, apolactoferrin,
apotransferrin, or iron nitrilotriacetate but not ferritin or bovine
serum albumin. There was no evidence for a role for parasite-derived
siderophores or proteolytic cleavage of ferritransferrin or
ferrilactoferrin in the acquisition of iron by promastigotes. Thus, L.
chagasi promastigotes can acquire iron from hemin, ferrilactoferrin,
or ferritransferrin. This capacity to utilize several iron sources may
contribute to the organism's ability to survive in the diverse
environments it encounters in the insect and mammalian hosts.
PMID: 8039896, UI: 94314443
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