Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT00568 (ascorbate)
 23,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical signs and changes in blood and rumen fluid, and the results of therapy are described in 35 cows suffering from bleeding abomasal ulcer. The most important pathological findings were moderate to severe anaemia with pale mucous membranes and tachycardia, dark coloured to black faeces, a disturbed general condition and anorexia. Two of the cows were slaughtered immediately. The others were treated by the transfusion of several litres of blood and the intravenous administration of a solution containing sodium chloride and glucose and other drugs such as calcium solution, vitamin K, vitamin C and metoclopramide. Two animals died in spite of the treatment and three had to be slaughtered because of the deterioration in their condition. The other 28 cows recovered within a few days and their general condition, appetite and defecation returned to normal.
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PMID:Bleeding abomasal ulcers in dairy cows. 196 99

To study the overt toxicosis of intraperitoneally (IP)-administered single doses of cholecalciferol (D3), groups of male CF-1 mice (N = 12) were given graded doses of D3 in corn oil and observed for 21 days. There was a 2- to 4-day onset of signs, including ocular squinting, reluctance to move, lethargy, weakness, anorexia, hunched posture, rough haircoat, and dehydration. This was followed by tremors, coma, and death (large doses) or gradual recovery. Deaths occurred 3 days (larger doses) to 21 days after D3 injection. The linear regression of mortality probits on log10 dose was Y = 7.332X-10.653. The median lethal dose (LD50) of D3 and 95% confidence limits were 135.4 mg/kg (112.2-157.4 mg/kg). To screen potential antidotes against acute D3 toxicosis, groups of mice (N = 12) were given subcutaneous (SC) injections of various substances beginning 2 days after IP injection of a large dose of D3 (300 mg/kg). Substances were given once or twice daily in constant volumes of saline solution (66.8 ml/kg) for 7 days. Two control groups were given D3 but no treatment. They both had 91.7% mortality; their mean (+/- SD) survival time (MST: censored to 21 days observation) was 6.8 +/- 4.7 days and 10.3 +/- 7.0 days. Mortality and MST were not affected significantly (P greater than 0.05) by once-daily injection of saline solution, saline containing dexamethasone (DEX), or saline containing the following substances with or without DEX: ascorbate; citrate; dimercaptosuccinic acid; oxytetracycline; ZnSO4; or MgCl2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute intraperitoneal cholecalciferol (vitamin D3) toxicosis in mice: its nature and treatment with diverse substances. 253 55

Paraquat dichloride at 250 ppm in the diet was fed continuously to rats. Though no apparent effect of paraquat was observed until 10 d, some rats then began to show several symptoms such as diarrhea, anorexia, epistaxis, and hypokinesia, and in some cases rats died after this period. The biochemical examination of plasma components revealed appreciable changes in the concentrations of an acute-phase reactant protein and some vitamins that act as antioxidants. alpha-Cysteine proteinase inhibitor increased by 5-fold, and vitamin C and its radical increased by 1.5- and 1.7-fold, respectively, whereas alpha 1 proteinase inhibitor decreased slightly. Paraquat enhanced the cysteine proteinase inhibitor levels in lung, liver, and kidney by 6.2-, 6.0-, and 4.5-fold of control, respectively. Among three components of alpha-cysteine proteinase inhibitor, the T kininogen level of treated rat plasma was about eight-fold higher than control, whereas the high-molecular-weight kininogen level was unchanged. The large increment of T kininogen was also seen in lungs of the treated rats.
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PMID:Acute-phase reactant proteins and antioxidants in rats intoxicated chronically with paraquat. 752 39

Biochemical and gross pathological effects of diquat were studied with special attention to cysteine proteinase inhibitor level which was often increased in acute and chronic disorder. Diquat was fed continuously to rats at the dose of 1000 ppm in the diet. After 10 days, anorexia and severe diarrhea were observed but epistaxis and hypokinesia were not apparent. The rats were killed after feeding the diet for 13.5 days and plasma components such as acute phase reactant proteins and some vitamins which act as antioxidants were examined. The results showed that alpha-cysteine proteinase inhibitor (alpha-CPI) increased to 9-fold and vitamin C radical increased to 1.6-fold, whereas alpha 1 proteinase inhibitor (alpha 1-PI) decreased to 0.9-fold and vitamins C and E were the same as the control. Among three components of alpha-CPI, the T kininogen level in intoxicated rat plasma was about 20-fold, whereas the high molecular weight kininogen level was about 2-fold of the control. Diquat also enhanced the cysteine proteinase inhibitor (CPI) level to 20-fold in kidney and to 7- to 10-fold in the other organs. The large increment of T kininogen in these organs was also confirmed immunologically. The kidney showed a granular degeneration and its weight increased to 1.2-fold of control. The other organs showed neither gross pathological alteration nor weight change, compared with the control. The diquat distribution was highest in spleen and next highest in kidney among several organs. These results were compared with those caused by paraquat.
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PMID:Diquat increases cysteine proteinase inhibitors greatly in rat plasma and tissues. 765 36

The most consistent toxic effects of dioxin-type chemicals are hyperlipidemia, body weight loss (particularly body fat loss), anorexia, changes in carbohydrate metabolism, and lipid peroxidation. The biochemical systems particularly affected are lipoprotein lipases, low-density-lipoprotein receptors, glucose transporter proteins (GLUTs), vitamin C uptake, and insulin secretion. Some of these biochemical changes occur at very low doses, and some effects can last for long time periods. To provide a mechanistic explanation for such actions of dioxins, available experimental evidence has been reviewed. The most recent discovery indicates that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) directly acts with isolated cytosolic aryl-hydrocarbon (Ah) receptor under cell-free conditions even without the presence of the nucleus and is capable of activating key protein kinases that are involved in the growth factor signal-transduction pathway. The resulting activation of primary-response transcription factors in the nucleus appears to play a key role in coordinating vital cell program shifts, including lipid metabolism.
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PMID:Mechanism of action of dioxin-type chemicals, pesticides, and other xenobiotics affecting nutritional indexes. 787 40

The following review summarizes important facts about the water-soluble vitamins thiamin, riboflavin, B6, B12, folate and vitamin C and the fat-soluble vitamins A, D, E and K with regard to their effects, the critical stability and the most frequent deficiencies. Water, oxygen and light are the most important factors which have the ability to destroy water-soluble vitamins. Because the first clinical signs of vitamin deficiencies are unspecific, e.g. anorexia, sleeping disturbances, little power of concentration and irritability, they are often not diagnosed early enough. Therefore, the dietitians should control and if needed alter the dietary habits in order to improve vitamin supply, in particular in elderly people, patients with long-term hospital stay, vegetarians and young women with eating disorders.
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PMID:[Significance of vitamins in nutrition counseling]. 807 88

It has been suggested that dopamine in nucleus accumbens is involved in the process of enabling organisms to overcome work-related response costs. One way of controlling work costs with operant schedules is to use fixed ratio schedules with different ratio requirements. In the present study, the effects of nucleus accumbens dopamine depletions were investigated using six schedules: fixed ratio 5, 20, 50, 100, 200, and 300. In the first three schedules the food reinforcement consisted of one 45 mg food pellet per ratio completed. In the remaining schedules the food reinforcement per ratio completed was increased to two pellets for fixed ratio 100, four pellets for fixed ratio 200, and six pellets for fixed ratio 300. All rats were trained extensively prior to surgery, and rats were able to maintain high levels of responding on all schedules up to the fixed ratio 300. After training, rats were injected with either ascorbate vehicle or 6-hydroxydopamine into the nucleus accumbens. Rats were tested post-surgically on each of the schedules, with 3 days of testing per schedule. Rats with nucleus accumbens dopamine depletions exhibited behavioral deficits that were highly dependent upon the ratio value. There were small and transient effects of dopamine depletion on fixed ratio 5 lever pressing, but as the ratio value got larger the impairment became greater. On the fixed ratio 20 and 50 schedules, response rates were partially reduced in dopamine-depleted rats. Responding on the fixed ratio 200 and 300 schedules was severely impaired, and on the last day of fixed ratio 300 testing no dopamine-depleted rats obtained a single reinforcer. These data are consistent with previous reports that accumbens dopamine depletions enhance 'ratio strain', making rats more sensitive to high ratio values. The induction of ratio strain by dopamine depletions does not appear to be related to a loss of appetite, and seems to be relatively independent of the baseline rate of responding and the overall density of food reinforcement across the session. We conclude that dopamine in nucleus accumbens may be important for enabling rats to overcome behavioral constraints such as work-related response costs, and may be critical for the behavioral organization and conditioning processes that enable animals to emit large numbers of responses in the absence of primary reinforcement.
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PMID:Nucleus accumbens dopamine depletions make animals highly sensitive to high fixed ratio requirements but do not impair primary food reinforcement. 1153 Feb 24

Despite a dramatic increase in research on eating-related pathologies, gaps remain in our understanding of the factors responsible for the development and maintenance of dysfunctional attitudes and behaviour related to weight and eating among adolescents. A study was therefore conducted to compare eating and weight concerns among underweight, normal-weight and obese affluent adolescent girls in New Delhi. The sample comprised fifty underweight, fifty normal-weight and thirty obese girls, 16-18 years of age. Information was collected about their body image perception, weight concerns and eating attitudes by a well-structured questionnaire. Dietary intake was determined by 24 h recall and a food-frequency questionnaire. Body size was adjudged by measurements of weight, height, waist, hip and mid upper arm circumferences, and the BMI and waist : hip ratio were determined. Of the subjects, 99.2 % had a gynoid pattern of fat distribution. Concerns about excess weight were prevalent among the adolescent girls, even among those who were normal-weight and underweight. The level of satisfaction with body size decreased with increase in weight. Dieting behaviour was reported in a higher number of obese (76.6 %) compared with normal-weight (38 %) and underweight (14 %) girls. Of the obese girls, 43.3 % were found to be at a significantly (P=0.00109) greater risk of developing anorexia in the future. Characteristic dietary features of adolescence, such as missing meals, snacking and eating out, were observed. While the diets of most of the subjects were adequate in Ca, thiamin, riboflavin and vitamin C, they were found to be deficient in energy, protein, Fe, niacin, vitamin A and fibre. Thus, it is important to recognize that weight concerns and dissatisfaction with body size may pose a threat to a healthy nutritional state, and may develop into precursors of a later eating disturbance.
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PMID:Affluent adolescent girls of Delhi: eating and weight concerns. 1159 Dec 42

An 80 year old man, who relied on a home based meals-on-wheels service was admitted to hospital with non-specific symptoms, but had clinical and biochemical evidence of scurvy. Subsequently, all new admissions (n=37) to the department over a three week period were assessed for evidence of undernutrition. It was found that 73% had hypovitaminosis C, with 30% having concentrations suggestive of scurvy. There were no significant associations between level of vitamin C and type of accommodation, food provision, or age. The commonest symptom associated with vitamin C deficiency was anorexia, but overall, there was a paucity of clinical signs associated with vitamin C deficiency. The possible associations of vitamin C deficiency in the elderly are discussed.
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PMID:Will an orange a day keep the doctor away? 1215 75

A child responds to a deficiency of an essential nutrient either by continuing to grow and consuming body stores with eventual reduction in the bodily functions (Type I) or by reducing growth and avidly conserving the nutrient to maintain the concentration of the nutrient in the tissues (Type II). Examples of Type I nutrient deficiency are anemia (iron deficiency), beri-beri (thiamin deficiency), pellagra (niacin or nicotinic acid deficiency), scurvy (vitamin C or ascorbic acid deficiency), xerophthalmia (vitamin A or retinol deficiency) and iodine deficiency disorders. Diagnosis is relatively simple via clinical symptoms and measurement of the concentration of the nutrient itself. There are no characteristic symptoms to distinguish which Type II nutrient deficiency an individual has; all deficiencies result in the poor growth, stunting, and wasting generally ascribed to protein-energy malnutrition. In Type II, growth stops, the body starts to conserve the nutrient, and its excretion falls to very low levels. In severe deficiency the body may start to break down its own tissues and the reduction of appetite accompanies this condition. An animal can die from zinc deficiency even though it is has a normal concentration of zinc in its tissues, but it can respond rapidly to small amount of dietary zinc. The mechanisms by which the body stops growing in response to nutritional lack are similar to the hormonal picture seen in endocrine disease (reduction of the production of the hormonal mediators of growth, down-regulation of receptors, and reduction of protein synthesis). Growth failure is the clinical sign characteristic of a diet deficient in protein, zinc, magnesium, phosphorus, and potassium. Wasting may be also ascribed to toxins, infection, worms, or persistent diarrhea. Anorexia is another common response in nutrient deficiency. Only a supplementation diet with a balance of nutrients will promote rapid recovery.
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PMID:Specific deficiencies versus growth failure: type I and type II nutrients. 1234 13


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