Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although glucose-6-phosphate dehydrogenase deficient individuals may suffer (sometimes fatally) from favism, a high incidence of this trait occurs in many Mediterranean populations. This apparent paradox is explained on the basis of a synergistic interaction between favism and G-6-PD deficiency that provides increased protection against malaria compared to that of the G-6-PD deficiency alone. This relationship is analogous to that between various hemoglobins and malaria in that there is selection for a more severe trait if it provides more protection against malaria.
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PMID:Malaria, favism and glucose-6-phosphate dehydrogenase deficiency. 110 56

The frequency of PC allele for acid phosphatase in fourteen Sardinian villages correlates positively with the altitude and negatively with past malarial morbidity and GdMed prevalence. The susceptibility towards hemolytic favism in Sardinian males with G6PD deficiency is dependent on the erythrocyte acid phosphatase and thalassemia phenotypes. Thalassemia trait exerts a protective action only in subjects carrying PA allele for acid phosphatase. The data suggest that the gradient for malaria morbidity directly or indirectly, through interactions with thalassemia and G6PD polymorphisms, mediated by the habit of eating Vecia faba, may have had a significant role in determining the heterogeneous distribution of acid phosphatase polymorphism in Sardinia. Besides malaria, other environmental factors related with altitude seem to have been very important in shaping the present pattern of distribution of both acid phosphatase and G6PD polymorphisms in Sardinia.
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PMID:Red cell acid phosphatase: another polymorphism correlated with Malaria? 118 Mar 55

Favism, a hemolytic condition associated with fava bean consumption among the glucose-6-phosphate dehydrogenase (G6PD) deficient persons, is well described in the Middle East and Mediterranean areas. However, it is not well documented among the Thais or other Southeast Asians. It is possible that it does exist but that hemolysis which develops is of very minor degree and thus escapes clinical detection. This cross-sectional study hypothesizes that if the fava bean and G6PD deficiency interact in the Thai population, they should cause a significant difference in hematocrit level. The study was carried out in a community hospital in a malaria endemic area. We found that there was a trivial difference of the hematocrit (approximately 1%) which was too small to warrant any clinical significance after controlling for the extraneous effects of age, sex, use of malaria chemoprophylaxis, falciparum infection, use of analgesics/antipyretics and admission status of the patients (p = 0.668). This may be due to the presence of different G6PD mutants to those found elsewhere or due to different consumption patterns of fava beans among the Thais compared to people in other areas with high prevalence of G6PD deficiency.
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PMID:G6PD deficiency and fava bean consumption do not produce hemolysis in Thailand. 194 76

In this study, we have examined P. falciparum development in untreated normal or G6PD deficient erythrocytes as well as in parasitized cells exposed to isouramil--a fava bean extract known to induce oxidant stress in G6PD deficient erythrocytes (a condition known as favism), to diamide--a thiol oxidizing agent and to crisis form factor (CFF)--a non-immunoglobulin product found in the sera of man immune to malaria. We observed a significant retardation in intraerythrocytic development of parasites cultured in the G6PD deficient cells in comparison with parasites grown in the normal ones. Plasmodia within the G6PD deficient erythrocytes were markedly more sensitive to the inhibitory activity of CFF or the oxidizing agents diamide and isouramil. Mature stages of the parasites in both normal and G6PD deficient erythrocytes were more vulnerable than young ring forms, to oxidizing agents. The overall results show that the genetic trait of the host cell and the degree of maturation of the plasmodia are both crucial factors in determining the sensitivity of the parasite to oxidant stress.
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PMID:Inhibition of the intraerythrocytic development of Plasmodium falciparum in glucose-6-phosphate dehydrogenase deficient erythrocytes is enhanced by oxidants and by crisis form factor. 306 18

BCNU [1,3-bis(2-chloroethyl)-1-nitrosourea] and its less toxic derivative HeCNU [1-(2-chloroethyl)-3-(2-hydroxyethyl)-1-nitrosourea] are clinically-used antitumour drugs. In erythrocytes BCNU is a highly specific inhibitor of the enzyme glutathione reductase [H. Frischer and T. Ahmad, J. Lab. clin. Med. 89, 1080 (1977)]. When treating erythrocytes in vitro, 50% enzyme inhibition was obtained with 1 microM BCNU or 3 microM HeCNU within 2 hr. The two drugs were used for preparing red cell populations with various levels of glutathione reductase activity; complete inhibition (greater than or equal to 98%) was only achieved when the medium contained glucose as a source of reducing equivalents. The erythrocytes were then tested in drug-free media as host cells for the malaria parasite Plasmodium falciparum. In the range of 0-300 mU/ml cells, there was a correlation between glutathione reductase activity and parasite growth; erythrocytes with an activity of less than 20 mU/ml did not serve as host cells for P. falciparum at all although these erythrocytes were viable. When the culture medium was supplemented with 20 mM glutathione (GSH), parasite growth was normal irrespective of the glutathione reductase level in the erythrocytes. This is consistent with the finding that poisoning glutathione reductase led to a 10-fold decrease of the cytosolic GSH level. Our results corroborate the concept that intraerythrocytic inhibition of glutathione reductase mimicks the biochemistry of drug-sensitive glucose-6-phosphate dehydrogenase deficiency (favism), an inherited condition which confers protection from malaria.
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PMID:Glutathione reductase-deficient erythrocytes as host cells of malarial parasites. 327 13

There are important interactions between disease and organic evolution, between disease and cultural evolution, and between all three. Social behaviour influences disease and is influenced by it. Disease and disease mortality are woven into the complex of behavioural and physiological reactions to the stresses of overpopulation, which act to reduce population size. These principles are illustrated with reference to a number of diseases, including vitamin D imbalance, phenylketonuria, lactose intolerance, malaria, sickle cell anaemia, favism, plague, yellow fever, syphilis, ergot poisoning, kuru, and the sweating sickness.
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PMID:Evolutionary and social aspects of disease. 668 92

Glucose-6-phosphate dehydrogenase (G6PD) is expressed in all tissues, where it catalyses the first step in the pentose phosphate pathway. G6PD deficiency is prevalent throughout tropical and subtropical regions of the world because of the protection it affords during malaria infection. Although most affected individuals are asymptomatic, there is a risk of neonatal jaundice and acute haemolytic anaemia, triggered by infection and the ingestion of certain drugs and broad beans (favism). A rare but more severe form of G6PD deficiency is found throughout the world and is associated with chronic non-spherocytic haemolytic anaemia. Many deficient variants of G6PD have been described. DNA sequence analysis has shown that the vast majority of these are caused by single amino acid substitutions. The three-dimensional structure of G6PD shows a classical dinucleotide binding domain and a novel beta + alpha domain involved in dimerization.
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PMID:Glucose-6-phosphate dehydrogenase deficiency. 1091 76

This review explores the relation between evolution, ecology, and culture in determining human food preferences. The basic physiology and morphology of Homo sapiens sets boundaries to our eating habits, but within these boundaries human food preferences are remarkably varied, both within and between populations. This does not mean that variation is entirely cultural or learned, because genes and culture may coevolve to determine variation in dietary habits. This coevolution has been well elucidated in some cases, such as lactose tolerance (lactase persistence) in adults, but is less well understood in others, such as in favism in the Mediterranean and other regions. Genetic variation in bitter taste sensitivity has been well documented, and it affects food preferences (eg, avoidance of cruciferous vegetables). The selective advantage of this variation is not clear. In African populations, there is an association between insensitivity to bitter taste and the prevalence of malaria, which suggests that insensitivity may have been selected for in regions in which eating bitter plants would confer some protection against malaria. Another, more general, hypothesis is that variation in bitter taste sensitivity has coevolved with the use of spices in cooking, which, in turn, is thought to be a cultural tradition that reduces the dangers of microbial contamination of food. Our evolutionary heritage of food preferences and eating habits leaves us mismatched with the food environments we have created, which leads to problems such as obesity and type 2 diabetes.
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PMID:The gourmet ape: evolution and human food preferences. 1965 37