No abstract

Further studies of protein catabolism and renal function in autism are required to ascertain the relevance of decreased spot urinary creatinine excretion identified in this preliminary study. Issues regarding the use of single urine creatinine measurements and associated confounding variables are discussed in light of the findings, together with recommendations to use other internal or external standards for the quantification of urinary compounds in PDD research.

Purpose: There can be wide variation in individual responses to dietary components and also in detoxification of drugs and environmental compounds. This article seeks to explore some of the factors underlying these findings. Design: Glutathione-S-transferases (GST isoforms) link reactive chemical species with glutathione; they are polymorphic in human populations and are cytosolic and found in most tissues of the body. Their activity is modulated by dietary components, as is the activity of the cytosolic sulfotransferase (SULT) isoforms which catalyse sulfation of drugs and endogenous compounds such as steroids. Fruit and vegetable cytosols were incubated with cytosols from rat and human tissues and the activities of GST and SULT enzymes were measured. Materials and methods: Fresh fruits and vegetables were homogenised in distilled water to give 10% solutions. These were then added to supernatants from human and rat tissues, prepared by homogenising the tissue in ice-cold phosphate buffer and centrifuging. The activities of the SULT and GST enzymes were measured by standard methods. Results: Different fruits and vegetable cytosols had different effects on cytosols from the various tissues; Cruciferae cytosols activated the GST isoforms found in gut cells but inhibited GSTs in the liver; these were activated by tomato (which also activated kidney GST) and grape. Onion and banana both activated heart GST. Generally, the results were complex but suggested that gut GST isoforms were more readily activated by fruit and vegetable cytosols than GSTs from other tissues. The SULT isoforms 1A1 and 1A3 were inhibited by a wide range of fruits and vegetables, especially banana, cruciferae, onion and peppers; these results may be relevant to breast cancer, where inhibition of SULT 1A1 would lead to higher levels of estrogens. Patients with allergies had reduced plasma sulfate levels, probably due to down-regulation of sulfate-producing enzymes by cytokines generated in chronic inflammatory states. Conclusion: The activity of detoxifying pathways controlled by enzymes such as GSTs and SULT isoforms can be modulated by diet and physiological states.

1. Fasting levels of plasma cysteine, plasma sulphate and the plasma cysteine/sulphate ratio were measured in patients with primary biliary cirrhosis and compared with those in patients with other liver disease, general intensive therapy unit patients and healthy subjects. 2. Plasma cysteine was significantly elevated in patients with primary biliary cirrhosis (median 0.364 nmol/mg of protein, P < 0.0001) and patients with other liver disease (median 0.445 nmol/mg of protein, P < 0.0001), compared with healthy control subjects (median 0.125 nmol/mg of protein) and increased progressively with the severity of liver disease. Plasma cysteine was also elevated in intensive therapy unit patients (median 1.564 nmol/mg of protein) compared with healthy control subjects (P < 0.0001) and patients with other liver disease (P < 0.0001). 3. Plasma sulphate was reduced significantly only in patients with primary biliary cirrhosis (median 0.822 nmol/mg of protein) compared with healthy control subjects (median 1.37 nmol/mg of protein, P < 0.05). There was no significant difference in plasma sulphate between disease groups. 4. The plasma cysteine/sulphate ratio was significantly elevated in patients with primary biliary cirrhosis (median 0.448, P < 0.0001) and patients with other liver diseases (median 0.394, P < 0.0001) compared with healthy control subjects (median 0.095). The ratio was also elevated in intensive therapy unit patients (median 1.650, P < 0.0001) compared with healthy control subjects and liver disease groups (P < 0.0001). 5. In conclusion, cysteine rises in primary biliary cirrhosis and other forms of liver disease. This effect is not specific to liver disease, since cysteine is elevated in an heterogeneous group receiving intense care.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract