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Biomedical subjects

C O Enwonwu

Publications and source records attributed to C O Enwonwu.

At least 55 records · Page 3Linked to original sources
PubMed1988

Nutritional support in sickle cell anemia: theoretical considerations.

Despite the clinical diversity of sickle cell anemia (HbSS) this autosomal recessive disorder, often characterized by a 6- to 20-fold increase in destruction rates of the red blood cells (RBC) without a corresponding increase in synthesis, is essentially a chronic hypermetabolic condition. The stress of HbSS produces caloric inefficiency and a marked increase in resting metabolic rate. Nitrogen metabolism is set at a higher than normal dietary intake, and data are still incomplete regarding the possibility that this genetic disorder may have special amino acid requirements. The physiologic needs for most vitamins and essential mineral elements are increased because of the elevated dietary requirements for energy and nitrogen. Many of these micronutrients, especially α-tocopherol, ascorbic acid, retinol, zinc, and selenium, are free radical scavengers, and thus play crucial roles in retarding premature aging of RBCs caused by peroxidation of the membrane. Evaluation of the dietary requirements of the HbSS victim must also take into account the variable, often age-related, increase in nutrient losses after functional impairment in organs, such as the kidneys, which are usually elicited by repeated vaso-occlusive insults.

Anemia, Sickle Cell↗
PubMed1987

Differential effect of total food withdrawal and dietary protein restriction on brain content of free histidine in the rat.

Total withdrawal of food from young rats for 72-120 h produced an increase in brain content of free histidine which was less pronounced than the effect of prolonged dietary protein deficiency. The data suggested that the elevated brain content of histidine in both fasting and protein deficiency was due partly to increased plasma level of the amino acid but mainly to diminished plasma concentrations of the neutral amino acids known to share the same transport system across the blood-brain barrier. The results also support the idea that total starvation, and most likely, prolonged caloric restriction, like protein malnutrition, elicit increased formation of histamine in brain since the key regulatory enzyme, L-histidine carboxylase (EC 4.1.1.22) functions at less than maximal efficiency under normal brain levels of histidine. These findings in the rat are probably relevant to the human in view of evidence that the Km of blood-brain barrier neutral amino acid transport in the latter is low and therefore similar to the situation in the rat.

Animals↗
PubMed1987

Pathophysiological implications of increased brain burden of histamine in protein malnutrition.

The complex syndrome of protein-energy malnutrition (PEM) in weanling children, usually complicated by concurrent presence of numerous adverse environmental factors, is a chronic stressful situation which elicits a number of neuroendocrine and metabolic adjustments. Histidine metabolism is severely impaired in PEM in children and in experimental animals, and evidence from the latter indicate markedly increased body burden of histamine. The brain is the organ most prominently affected. Although data are still incomplete, histamine conforms with most criteria required of a neurotransmitter. Histamine interacts with other neuroregulatory substances in modulating many neuroendocrine and vegetative processes. Some of the prominent pathophysiological features associated with PEM in children such as increased circulating cortisol, defective thermoregulation, fluid/electrolyte imbalance, impaired immunity, reduced cardiac output with prolongation of systemic recirculation time, and apathy bordering on a clinical state of depression are consistent with the known effects of histamine as determined by neurochemical and neuropharmacological studies. It is suggested that studies of histamine status in human PEM, and the functional relationships between markedly elevated level of this amine with other neuroregulatory substances, will shed more light on the complex pathogenesis of the nutritional syndrome.

Adipose Tissue, Brown↗
PubMed1987

Potential health hazard of use of mercury in dentistry: critical review of the literature.

This report examines recent publications on the health hazards associated with the use of mercury in dentistry with emphasis on the release of mercury vapor from silver-amalgam restorations. While there is consistent evidence indicating release of mercury vapor from the restorations during chewing, tooth brushing, and other oral activities, proof of a causal link of this specific source of the heavy metal to any major human health problem is lacking. Several gaps in our knowledge of the metabolism of mercury vapor in the human militate against accurate prediction of the potential health significance of chronic exposure to this source of mercury, and some relevant lines of research have been recommended.

Body Burden↗
PubMed1987

Ijanikin: a study of environmental health in a rural Nigerian community.

Ijanikin is a typical Yoruba village in the rain forest belt area of Southern Nigeria. The childhood years in this community are fraught with the danger of numerous communicable diseases, compounded by inadequate supply of good quality foods to meet normal requirements and allow a margin of safety for the stress of infections. Overcrowding and poor ventilation in the houses are important factors in the spread of communicable diseases, while poor sanitation and deficient personal hygiene account for the heavy burden of intestinal parasitoses. Improvement in the health of this and other similar rural communities would require the provision of clean water supply, installation of essential sanitary facilities, provision of adequate food supply, and a well-planned and carefully executed health education programme.

Animals↗
PubMed1985

Infectious oral necrosis (cancrum oris) in Nigerian children: a review.

The devastating orofacial gangrenous disease known as cancrum oris (noma) is still commonly seen in underprivileged Nigerian children. These children are usually victims of such stressors as chronic malnutrition, numerous endemic communicable diseases and severe adverse physical conditions which may lead to depletion of their adaptive resources or produce physiological maladaptation to additional stressors. Measles is the most common infection preceding the development of noma in Nigerian children. Acquired immunodeficiency as well as the impaired endocrine balance of the chronically malnourished permits, for example, widespread infection with the measles virus. Anergy resulting from the combination of malnutrition and measles virus infection promotes selective overgrowth and invasion by an infective consortium consisting of anaerobic organisms and other species capable of elaborating necessary growth factors for the former. Because of the pre-existing depletion of adaptive physiologic resources in the malnourished child, the infection is not readily contained locally as necrotizing ulcerative gingivitis but instead spreads rapidly to the next naturally occurring anatomical barriers. This is then followed by continuing necrosis and possible sequestration as exemplified by noma.

Animals↗
PubMed1984

The role of dietary aflatoxin in the genesis of hepatocellular cancer in developing countries.

Impaired activity of the liver microsomal mixed-function-oxidase (MFO) system is characteristic of protein malnutrition. It explains the accumulation of aflatoxin (AFB1) in livers of kwashiorkor victims, whose staple foods are usually heavily contaminated with this fungal toxin. Dietary rehabilitation of such children with high-protein foods not only increases the activity of the liver MFO system but also stimulates DNA replication and rapid regeneration of liver cells. Under such circumstances highly reactive metabolites of AFB1, such as the AFB1-epoxide, can produce malignant transformation of the cells by binding covalently with genetic macromolecules. Alternating cycles of food shortage and sufficiency, which usually characterise impoverished communities, and liver-cell hyperplasia stimulated by the non-genetic cytotoxic effects of AFB1 or parasitic infestation promote rapid replication of the transformed cells.

Aflatoxin B1↗
PubMed1984

Distribution of hepatic ribosomes between different functional states in well-fed and protein-energy-deficient rats.

Electron microscopy of hepatic cells from protein-deficient young rats revealed extensive breakdown of the rough endoplasmic reticulum into fragments and vesicles whose membranes appeared fully studded with ribosomes. Additionally, there was biochemical evidence of marked disaggregation of polysomes (n greater than 2), and this was more prominent in the membrane-bound than in free polysomes. Protein malnutrition increased the proportion of membrane-bound ribosomes which were salt-releasable and therefore temporarily non-functional. It has been concluded that disaggregation of membrane-bound polysomes induced by malnutrition does not necessarily imply detachment of the monomeric ribosomes from the endoplasmic membrane into the pool of free ribosomes, which probably has a separate polyribosomal cycle.

Animals↗
PubMed1983

Rapid development of oedema and defective brain histidine metabolism in young guinea pigs fed protein-energy deficient diet.

Male weanling guinea pigs were fed ad libitum a 3% pelleted casein diet supplemented with ascorbic acid while control animals were pair-fed a standard guinea-pig chow. Oedema was observed in some of the former group as early as the 2nd week and became very prominent by the end of the 3rd week. The malnourished group was characterized by reduced plasma albumin level and some disaggregation of hepatic polyribosomes but these showed no correlation in time with development of oedema. The pool of plasma essential amino acids were markedly reduced as early as Day 7, and most prominently affected were threonine, valine, isoleucine, leucine and arginine. Plasma histidine level was not significantly affected by malnutrition. Associated with early distortion of plasma aminogram was a pronounced increase (+176%) in free corticosteroid level by Day 7. Plasma concentration of aldosterone was significantly elevated in the malnourished guinea-pigs in comparison with the control group of the same age. Brain levels of free amino acids were not as extensively altered by malnutrition as was the case in plasma. At Day 7, only arginine, leucine and isoleucine among the essential amino acids, were significantly reduced while phenylalanine level was markedly increased. Histidine and its dipeptide homocarnosine as well as ornithine were the ninhydrin-positive substances in the brain most severely affected. By Day 14, the levels of histidine and homocarnosine were +71% and +58% respectively higher than the control values. Since the rate limiting factor in the synthesis of the putative neurotransmitter histamine in brain is the availability of the precursor amino acid histidine, the possible implications of pronounced increase in brain level of free histidine in experimental protein-energy malnutrition were discussed in the light of the known role of histamine as one of the neurotransmitters influencing the function of the anterior pituitary through regulation of release of the hypothalamic hypophysiotropic hormones.

Adrenal Cortex Hormones↗
PubMed1977

Protein-energy malnutrition in infant non-human primates (Macaca nemestrina). I. Correlation of biochemical changes with fine structural alterations in the liver.

Male infant pigtail monkeys (Macaca nemestrina) aged 6-9 months and born in captivity were fed restricted amount of either an adequate protein diet (20% casein) or a protein-deficient diet (2% casein). After 3-5 months of receiving the low protein containing diet, ultrastructural evaluation of hepatic parenchymal cells revealed extensive fatty metamorphosis, marked fragmentation and vesiculation of the rough endoplasmic reticulum, some evidence of distension of the nuclear membrane, variable degree of mitochondrial polymorphism and gigantism, increased intracytoplasmic accumulation of glycogen particles and enhanced prominence of collagen fibres in the intercellular and perisinusoidal spaces. Biochemical studies indicated severe distortion in the plasma profile of free amino acids by Week 10 of malnutrition, with a prominent decrease in valine/glycine ratio (9% in the malnourished animals compared to a ratio of 55-63% in the control group). While plasma concentration of glycine was elevated above baseline value throughout the period of malnutrition, the level of alanine showed an initial rise followed by a significant drop (-58% at Week 20). Although showing wide individual variation, plasma level of corticosteroid in general tended to increase with duration of protein malnutrition, an observation consistent with the accumulation of glycogen and enlargement of mitochondria in the hepatic cells.

Adrenal Cortex Hormones↗
PubMed1975

Functional variations in the ultrastructure of the thyroid gland in malnourished infant monkeys.

Healthy male pigtail monkeys (Macaca nemestrina) were procured at the age of 6-9 months, and fed either a 20 percent casein diet or a diet containing 2 percent casein as the sole source of protein. After 3-5 months, the malnourished monkeys developed many features usually associated with the clinical syndrome of marasmic kwashiorkor as seen in socioeconomically underpriviledged societies. Ultrastructural evaluation of thyroid gland revealed that dietary protein-calorie deficiency produced marked reduction in follicular cell height, conspicuous decrease in the number of apical filamentous microvilli, and a relative scarcity of the apical microvesicles as well as other pale staining colloid vesicles compared to findings on control glands. The electron-dense lysosomelike granules did not appear particularly affected, although in some sections they seemed to have increased in number and were located mainly in the basal portion of the cells, These electron-dense granules often displayed marked lack of homogeneity in regard to their structure in the malnourished glands. Most of these morphologic alterations have been noted frequently in thyroid glands of hypophysectomized animals, or in glands suppressed by the administration of thyroxine, and are therefore highly indicative of thyroid hypofuction in this animal prototype of human protein-calorie malnutrition.

Amino Acids↗