Effects of ammonia, nitrite and nitrate on hemoglobin content and oxygen consumption of freshwater fish, Cyprinus carpio (Linnaeus).

Lethal effects of nitrogenous compounds ammonia, nitrite and nitrate on freshwater fish Cyprinus carpio were studied and the static LC50 values obtained for these 3 toxicants for 24 hr were 0.80 ppb, 171.36 ppm; 1075.10 ppm and continuous flowthrough LC50 values for 24 hr were 0.72 ppb, 154.31 ppm; 967.63 ppm respectively. The fish were exposed to lethal concentrations to study the changes in hematological parameters and the rate of oxygen consumption. During the period of exposure general decline in the content of hemoglobin was observed. Methemoglobin content increased in case of nitrite exposure consequently the hemoglobin levels decreased drastically. It is also observed that rate of oxygen consumption decreased progressively with the increase of toxicant concentration and duration of the exposure.

Avaliação dos produtos da degradação oxidativa da Hb S nos genótipos SS, SF (S/beta0 talassemia) e AS, em comparação com hemoglobinas normais / Evaluation of the products from oxidative damage of Hb S in SS, SF (S/beta0 thalassemia) and AS genotypes compared to normal hemoglobins

A doença falciforme é um termo genérico usado para determinar um grupo de alterações genéticas caracterizadas pelo predomínio de hemoglobina (Hb) S. Os principais genótipos que compõem o grupo de doença falciforme são os seguintes: SS, SF [S/beta0 talassemia e S/persistência hereditária de Hb fetal (PHHF)], SFA (S/beta+ talassemia), SC, SD e SH (S/alfa talassemia). O presente trabalho analisa os resultados das avaliações de produtos provenientes da oxidação da Hb S, identificados pela concentração da metemoglobina e de eritrócitos com corpos de Heinz em dois genótipos da doença falciforme (SS e S/beta0 talassemia) e no traço falcêmico (AS), em comparação com o genótipo normal (AA). A análise dos produtos da degradação oxidativa da hemoglobina, evidenciados pelo aumento dos valores das médias referentes à concentração de metemoglobina e do número de eritrócitos com corpos de Heinz, está diretamente relacionada com o aumento da concentração da Hb S. Assim, a degradação oxidativa da hemoglobina decresce entre os genótipos estudados da seguinte forma: SS>SF>AS>AA. É importante destacar que as análises indicaram que a simples presença de Hb S no eritrócito, como é o caso do genótipo AS, é capaz de causar elevação da concentração de metemoglobina em 52,62% das amostras analisadas e de induzir a precipitação de corpos de Heinz em 73,68% dos casos estudados. Explicações referentes aos processos oxidativos e redutores das hemoglobinas estudadas são apresentados no texto. Destaca-se, entre os resultados apresentados, a identificação por meio de eletroforese em agarose alcalina da fração de globina alfa-livre em todas as amostras do genótipo SF provenientes de pessoas com Hb S/beta0 talassemia. É proposto um esquema para explicar a origem da globina alfa-livre, especialmente para o genótipo S/beta0 talassemia, e a importância da sua identificação no diagnóstico laboratorial de Hb S/beta0 talassemia.

Sickle cell disease is a generic term used to determine a group of genetic alterations characterized by a dominance of Hb S. The main genotypes which compose the sickle cell disease group are as follows: SS, SF (S/b0 thalassemia and S/Hereditary Persistence of Fetal Hemoglobin or HPFH), SFA (S/b+ thalassemia), SC, SD and SH (S/a thalassemia). This study analyzes the products resulting from the oxidization of hemoglobin, identified by the methemoglobin concentration and by red blood cells with Heinz bodies, in two sickle cell genotypes (SS and S/b0 thalassemia) and in the sickle cell trait (AS) compared with the normal genotype (AA). Analysis of the products resulting from hemoglobin oxidative damage, characterized by an increase in the mean levels of methemoglobin and of the number of red blood cells with Heinz bodies, which are directly related to the increase in the Hb S concentration. Thus, oxidative damage of hemoglobin diminishes among the studied genotypes in the following manner: SS>SF>AS>AA. It is important to stress that these results indicate that the simple presence of Hb S in the red blood cell, as in the AS genotype, is capable of increasing the methemoglobin concentration in 52.62% of the assessed samples and inducing the precipitation of Heinz bodies in 73.68% of cases. Elucidation of the oxidative and reductive processes of the studied hemoglobins is presented in the paper. Highlighted among the presented results is the identification, by means of alkaline agarose gel electrophoresis, of the free alpha globin fraction in all SF genotype samples originating from Hb S/b0 thalassemia individuals. A hypothesis to explain the origin of free alpha globin, especially in the S/b0 thalassemia genotype is proposed, as is the importance of its identification in the laboratorial diagnosis of S/b0 thalassemia.

Effect of cadmium and zinc-metallothionein on methemoglobin and nitric oxide in dimethylnitrosamine treated rats.

Protective effects of metallothionein (MT) have been studied against dimethylnitosamine (DMN) toxicity in laboratory rats. MT was induced by feeding rats on repeated sublethal doses of cadmium and zinc. These rats were subsequently administered DMN. Methemoglobin and nitric oxides, the established markers of DMN toxicity, were estimated in the blood samples of MT protected rats. Preinduction of MT decreased methemoglobin and ameliorated the generation of nitric oxides. Antioxidative effects of MT may have manifested these results, however, an effect on N-nitrosation is also speculated.

A Thai boy with hereditary enzymopenic methemoglobinemia type II.

Individuals with methemoglobin exceeding 1.5 g/dl have clinically obvious central cyanosis. Hereditary methemoglobinemia is due either to autosomal dominant M hemoglobins or to autosomal recessive enzymopenic methemoglobinemia. Four types of enzymopenic methemoglobinemia have been described. In addition to methemoglobinemia, individuals with type II, which is the generalized cytochrome b5 reductase deficiency, have severe and progressive neurological disabilities. Here we report a 3-year-old Thai boy with type II hereditary enzymopenic methemoglobinemia. He was born to a second-cousin couple. His central cyanosis was first observed around 10 months of age. His neurological abnormalities were seizures beginning at 1 year of age, microcephaly, and inability to hold his head up. His cardiovascular and pulmonary evaluations were unremarkable. Methemoglobin level by spectral absorption pattern was 18 per cent. A qualitative enzymatic assay confirmed the deficiency of the cytochrome b5 reductase enzyme. With this definite diagnosis, a prenatal diagnosis for the next child of this couple will be possible.

The use of primaquine in malaria infected patients with red cell glucose-6-phosphate dehydrogenase (G6PD) deficiency in Myanmar.

32 subjects with Plasmodium falciparum gametocytes, and 31 cases with Plasmodium vivax infection from two military hospitals (Lashio, Mandalay) were treated with quinine 600 mg three times a day for 7 days followed by primaquine 45 mg single dose for gametocytes and 45 mg weekly x 8 weeks for vivax malaria. Although screening of red cell glucose-6-phosphate dehydrogenase (G6PD) was done prior to primaquine treatment, G6PD deficient subjects were not excluded from the trial. 20 patients hemizygous for mild G6PD deficiency (GdB- variant), 2 patients hemizygous for severe deficiency (Gd-Myanmar variant) completed the trial. No case of acute hemolysis was observed in all 22 patients with two genotypes of red cell G6PD deficiency status. Therefore, a single dose of primaquine 45 mg and/or weekly for 8 weeks is adequate for the treatment of patients with P. falciparum gametocytes and/or P. vivax malaria ignoring these red cell G6PD enzyme deficient variants in Myanmar.

Evaluation of a micromethod for detection of G-6-PD deficiency.

A simple and inexpensive micromethod based on methaemoglobin reduction technique (MRT) for screening of glucose-6 phosphate dehydrogenase deficiency has been studied using reagent-impregnated curvettes incubated in a makeshift waterbath. The cuvettes shelf life has been tested upto nine months. As the test can be done with finger prick blood, it promises to be more acceptable in the field. The sensitivity of this is similar to classical MRT.