Base de dados : MedCarib
Pesquisa : D01.339 [Categoria DeCS]
Referências encontradas : 8 [refinar]
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  1 / 8 MedCarib  
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Fotocópia
Id: 15798
Autor: Doherty, Justin F; Golden, Michael H. N; Brooks, Stanley E. H.
Título: Peroxisomes and the fatty liver of malnutrition: an hypothesis 1-3
Fonte: Am J Clin Nutr;54(4):674-7, Oct. 1991.
Idioma: En.
Resumo: Peroxisomes play a role in hepatic ß-oxidation of fat, a process that results in the production of hydrogen per-oxide. The fatty infiltration of the liver that occurs in severely malnourished children remains unexplained. We observed an almost total absence of peroxisomes in the hepatocytes of these children. We suggest that lack of available peroxisomes could contribute to the development of fatty liver.(AU)
Responsável: JM3.1 - Médical Library
JM3.1; RC620.A1A4


  2 / 8 MedCarib  
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Id: 15702
Autor: Golden, Michael H. N; Ramdath, D. Dan; Golden, Barbara E.
Título: Free radicals and malnutrition
Autor: Dreosti, I. E(ed).
Título: Trace elements, micronutrients and free radicals.
Fonte: New Jersey; Humana Press; 1991.
Idioma: En.
Responsável: JM3.1 - Médical Library
JM3.1; Reprint Collection


  3 / 8 MedCarib  
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Fotocópia
Id: 13665
Autor: Ramdath, D. Dan.
Título: Antioxidant status of malnourished children.
Fonte: Kingston; s.n; May 1989. vii,288 p. tab.
Idioma: En.
Tese: Apresentada a University of the West Indies (Mona) para obtenção do grau de Doctor of Philosophy.
Resumo: Free radicals, by virtue of their reactive nature, could account for the clinical features of kwashiorkor. These chemical species are produced in excess only after antioxidant defences fall. The possibility of this situation occuring in children with kwashiorkor was therefore investigated. Whole blood glutathione (GSH) levels were significantly decreased in children with kwashiorkor and marasmic-kwashiorkor. This indicates the presence of an overwhelming pro-oxidant stress. At a GSH level of 1.90 moles/Irbc (6.80 µmoles/gHb) oedema could be diagnosed with a sensitivity, specificity and positive accuracy of greater than 90 percent. GSH correlated inversely with the degree of oedema (r = -0.69). In children with maramus GSH was normal. Erythrocyte concentrations of NADPtot were normal in all children. The percentage of this nucleotide in the oxidised form ( percentNADP+/NADPtot) was normal in children with maramus, but abnormally elevated in oedematous children. This means that there is an acute change in the cellular redox in oedematous children, and implies that the cellular environment is oxidising. The activities of erythrocyte glutathione reductase, glutathione S-transferase (GST) and glyoxalase I were either normal or markedly elevated. Riboflavin status was poor. The end products of detoxification by GST, urinary mercapturic acids (UMCA), were between 3 and 5 times higher than normal. There were no intergroup differences. This suggests that the body's burden of toxins is significantly increased. During recovery from malnutrition, children with maramus showed a rapid restoration of normal antioxidant status, whereas those with oedematous malnutrition did so only after loss of oedema. This was followed by progressive, and unexpected, deterioration in antioxidant status: plasma vit. E and GSH levels decreased, and UMCA levels remained elevated. It was reasoned that the high PUFA content (60 percent )of the recovery diet may be a source of oxidative stress. In a second study the recovery diet contained an oil (coconut), rich in saturated fatty acids. On this diet children maintained normal levels of vit.E and GSH, and UMCA decreased significantly. This confirmed the high PUFA diet as a source of oxidative stress. Collectively, these data suggest that free radicals are involved in the aetiology and pathogenesis of kwashiorkor. It is recommended that: (1) whole blood levels of GSH be used in the diagnosis of oedematous malnutrition, and (2) coconut oil and antioxidants be used to treat malnourished children (AU)
Responsável: JM23.1 - Main Library
JM23.1; U Thesis


  4 / 8 MedCarib  
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Fotocópia
Id: 13586
Autor: Golden, Michael H. N.
Título: The effects of malnutrition in the metabolism of children
Fonte: Trans R Soc Trop Med Hyg;82(1):3-6, 1988.
Idioma: En.
Responsável: JM3.1 - Médical Library
JM3.1; RC960.R6


  5 / 8 MedCarib  
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Fotocópia
Id: 11636
Autor: Bennett, Franklyn I; Morgan, Owen St. C; Golden, Michael H. N; Stennett Dawkins, Memory A.
Título: Plasma thiocyanate and free radicals in Jamaican neuropathy (tropical paraparesis
Fonte: West Indian med. j;36(3):163-5, Sept. 1987.
Idioma: En.
Resumo: Tropical spastic paraparesis (TSP) in West African countries is caused by a combination of excess cyanide from the ingestion of cassava and a deficiency of the sulphur-containing amino-acids required to detoxify the cyanide. Free radical damage to long axons has also been reported to result in damage similar to that seen in Jamaican TSP. To investigate the possibility that these mechanisms may be responsible for Jamaican TSP, venous blood from non-smoking blood donors and 22 patients with TSP were analysed for thiocyanate, superoxide dismutase and glutathione. Serum thiocyanate is an index of cyanide exposure. Superoxide damage is an important sulphur-containing peptiae. Levels of thiocyanate in the patients with TSP were similar to those in control patients. Glutathione was elevated in all the patients, and a superoxide dismutase activity was normal. The low levels of thiocyanate suggest that cyanide toxicity is not the primary cause of Jamaican TSP and, in any event, sufficient amounts of sulphur-containing amino-acids are present to detoxify cyanide. Free radical mechanisms are also unlikely to be responsible for damage to the neurons in these patients (AU)
Responsável: JM3.1 - Médical Library
JM3.1; R18.W4


  6 / 8 MedCarib  
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Fotocópia
Id: 8356
Autor: Brooks, Stanley E. H; Doherty, Justin F; Golden, Michael H. N.
Título: Peroxisomes and the hepatic pathology of childhood malnutrition
Fonte: West Indian med. j;43(1):15-17, Mar. 1994.
Idioma: En.
Resumo: Liver specimens obtained immediately after death from eight severly malnourished children were examined by electron microscopy, and compared with seven liver biopsy specimens from children who recovered from malnutrition. The liver cells from the fatal cases showed mitochondrial swelling, with coarse densities in the matrix, cholestasis, depletion of the endoplasmic reticulum and Golgi apparatus, diminished glycogen stores, prominent lipid deposits and focal cytoplasmic degradation. The nucleoli were enlarged. There was marked reducation in peroxisomes. In contrast, the biopsies from recovering children showed good cellular organisation, and a normal frequency of peroxisomes. Multiple factors, including sepsis, may lead to depletion of peroxisomes. Loss of peroximes may interrupt beta-oxidation of long-chain fatty acids and accentuate the accumulation of lipid. Moreover, a reduction in the concentration of catalase may remove one avenue for the detoxification of free radicals. As the concentration of other anti-oxidants, notably glutathione, is also reduced, free radical damage may occur, leading to lipid peroxidation of membranes, mitochondrial damage, pump failure and influx of water and electrolyted into the cell (AU)
Responsável: JM3.1 - Médical Library
JM3.1; R18.W4


  7 / 8 MedCarib  
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Fotocópia
Id: 5316
Autor: Golden, Michael H. N; Ramdath, D. Dan; Golden, Barbara E.
Título: Free radicals and malnutrition
Fonte: In: Dreosti, I. E. Trace elements, micronutrients, and free radicals. Totowa, Humana, 1991. p.199-221.
Idioma: En.
Responsável: JM3.1 - Médical Library
JM3.1; Reprint Collection


  8 / 8 MedCarib  
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Fotocópia
Id: 2307
Autor: Ramesar, C. T; Ramdath, D. Dan.
Título: Increased levels of malondialdehyde in urine and plasma from diabetic patients and smokers: evidence for free radical damage - abstract
Fonte: WEST INDIAN MED. J;46(Suppl 2):23, Apr. 1997.
Idioma: En.
Conferência: Apresentado em: Commonwealth Caribbean Medical Research Council 42nd Scientific Meeting, St. Maarten, Apr. 16 - 19 1997.
Resumo: Malondialdehyde [MDA] is a major end product of lipid peroxidation which causes tissue damage and its presence is often used as an indicator for free radical damage in tissues. MDA was therefore measured in the urine and plasma of 15 non-insulin dependent diabetics (NIDDM) between the ages of 33 and 67 (mean 52) years, 10 chronic smokers 29 - 33 years old and control group of 14 healthy individuals 17 to52 years old. The average age of both the normal controls and smokers was 32 years with an average Body Metabolic Index (BMI) of 24 in both groups and 26 in the diabetic group. (A table showing mean + SEM values for urinary and plasma malondialdehyde is shown in abstract). We conclude that diabetics and smokers have significantly (p<0.008) higher levels of urinary MDA than the controls. Plasma MDA levels were only significantly higher for the diabetic group. When corrected for muscle mass and BMI, urinary MDA levels for the two test groups were sigificantly (p<0.001) higher than normal. There was a good correlation between urinary MDA and plasma MDA (r=0.74), p<0.001, df= 21. These data suggest (1) NIDM and smokers have increased exposure to free radical damage (2) urinary MDA provides a good indicator of lipid peroxidation. (AU)
Responsável: JM3.1 - Médical Library
JM3.1; R18.W4



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