LIVER TRANSAMINASE ACTIVITY IN RIBOFLAVIN-DEFICIENT RATS

1962 ◽  
Vol 40 (8) ◽  
pp. 1065-1070 ◽  
Author(s):  
Sailen Mookerjea ◽  
S. C. Jamdar

Rats were deprived of riboflavin until there was established impairment of growth, hepatomegaly, and depletion of flavin–adenine dinucleotide and of catalase in the liver. Under these conditions there were increased concentrations of glutamic–aspartic and glutamic–alanine transaminases in the liver. With dietary depletion and repletion of protein the transaminase levels followed changes in liver size. Since the protein concentration in the liver was not affected, the level of transaminase was directly associated with the degree of anabolism. The changes in the glutamic–alanine transaminase were the more pronounced.

1962 ◽  
Vol 40 (1) ◽  
pp. 1065-1070 ◽  
Author(s):  
Sailen Mookerjea ◽  
S. C. Jamdar

Rats were deprived of riboflavin until there was established impairment of growth, hepatomegaly, and depletion of flavin–adenine dinucleotide and of catalase in the liver. Under these conditions there were increased concentrations of glutamic–aspartic and glutamic–alanine transaminases in the liver. With dietary depletion and repletion of protein the transaminase levels followed changes in liver size. Since the protein concentration in the liver was not affected, the level of transaminase was directly associated with the degree of anabolism. The changes in the glutamic–alanine transaminase were the more pronounced.


1966 ◽  
Vol 22 (12) ◽  
pp. 794-795 ◽  
Author(s):  
A. K. Chatterjee ◽  
S. C. Jamdar ◽  
B. B. Ghosh

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2780
Author(s):  
Andrzej Krajewski ◽  
Krzysztof Piorun ◽  
Dominika Maciejewska-Markiewicz ◽  
Marta Markowska ◽  
Karolina Skonieczna-Żydecka ◽  
...  

Background: Burned patients have an increased need for vitamin D supply related to the maintenance of calcium–phosphate homeostasis and the regulation of cell proliferation/differentiation. This study aimed to analyze the concentration of 25-hydroxycholecalciferol and its relationship with severe condition after burn injury. Methods: 126 patients were enrolled in the study. Patients were qualified due to thermal burns—over 10% of total body surface area. On the day of admission, the following parameters were assessed: 25-hydroxycholecalciferol concentration, total protein concentration, albumin concentration, aspartate transaminase activity, alanine transaminase activity, albumin concentration, creatinine concentration, c-reactive protein concentration, procalcitonin concentration, and interleukin-6 concentration. Results: Almost all patients (92%) in the study group had an improper level of vitamin D (<30 ng/mL), with the average of 11.6 ± 10.7 ng/mL; 17.5% of patients had levels of vitamin D below the limit of determination—under 3 ng/mL. The study showed that there are several factors which correlated with vitamin D concentration during the acute phase of burn injury, including: total protein (r = 0.42, p < 0.01), albumin, (r = 0.62, p < 0.01), percentage of body burns (r = 0.36, p < 0.05), aspartate aminotransferase (r = 0.21, p < 0.05), and c-reactive protein (r = 0.22, p < 0.05). We did not find any significant correlation between vitamin D concentration and body mass index. Conclusions: The burn injury has an enormous impact on the metabolism and the risk factors of the deficiency for the general population (BMI) have an effect on burned patients. Our study showed that concentration of 25-hydroxycholecalciferol is strongly correlated with serum albumin level, even more than total burn surface area and burn degrees as expected. We suspect that increased supplementation of vitamin D should be based on albumin level and last until albumin levels are balanced.


1977 ◽  
Vol 233 (5) ◽  
pp. E397
Author(s):  
C Muttart ◽  
R Chaudhuri ◽  
J Pinto ◽  
R S Rivlin

The incorporation of a subcutaneous injection of [14C]riboflavin (2.5 muCi/100 g body wt) into flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and flavins bound covalently to proteins was determined at 1, 6, and 18 h in liver, cerebrum, and cerebellum from progeny of normal and maternally riboflavin-deficient Holtzman rats. Radioactivity remaining as riboflavin was also determined under these circumstances. Experiments were initiated within 24 h of birth. In both groups of newborn rats, the incorporation of radioactive riboflavin into covalently bound flavins in liver and brain proceeded more slowly than into the other flavin fractions. In addition, radioactivity incorporated into covalently bound flavins comprised a relatively smaller proportion of the total amount incorporated in brain than in liver. In progeny of riboflavin-deficient dams, an increased rate of incorporation of riboflavin into all three flavin derivatives, particularly FAD, was observed in liver and brain, compared to results in normal progeny. These data provide evidence that maternal riboflavin deficiency enhances the incorporation of riboflavin into tissue flavins in liver, cerebrum, and cerebellum from newborn rats.


2009 ◽  
Vol 7 (4) ◽  
pp. 244-255 ◽  
Author(s):  
K. Hosoya ◽  
L. K. Lord ◽  
A. Lara-Garcia ◽  
W. C. Kisseberth ◽  
C. A. London ◽  
...  

Hepatology ◽  
1998 ◽  
Vol 27 (3) ◽  
pp. 868-872 ◽  
Author(s):  
Philippe Mathurin ◽  
Joseph Moussalli ◽  
Jean-Fran�ois Cadranel ◽  
Vincent Thibault ◽  
Fr�d�ric Charlotte ◽  
...  

1980 ◽  
Vol 14 (3) ◽  
pp. 253-261 ◽  
Author(s):  
M. J. L. Clapp

The bodyweight, food consumption and various biochemical and haematological parameters were measured in, and breeding and histological studies made of, groups of rats fed 6 different diets. All diets acceptably supported reproduction. 1 diet restricted body weight gain by 30%, and increased plasma alanine transaminase activity. Nephrocalcinosis was seen in females fed diets with a calcium: phosphorous ratio of <1. Levels of dietary protein were positively correlated with the incidence of renal pelvic dilatation in offspring at 7 weeks of age.


2019 ◽  
Vol 18 (3) ◽  
pp. 192-196
Author(s):  
Maria Panetta ◽  
◽  
Alex Brightmore ◽  
W Stephen Waring ◽  
◽  
...  

Chloroform is a recognised cause of acute liver injury, although now rarely encountered in clinical practice. We present a case of inhalational chloroform self-poisoning in a 47-year-old man that presented to hospital initially with reduced conscious level and later developed acute liver injury that was treated with intravenous acetylcysteine. This paper reviews the existing literature and presents a summary of the mechanisms of chloroform hepatotoxicity. Published cases show that there is a characteristic delay of 24 to 48 hours between chloroform exposure and elevation of liver transaminase activity. Therefore, clinicians need to provide an appropriate duration of monitoring in order to detect the occurrence of this important toxic effect.


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