Sodium selenite (Na2SeO3) is the selenium form used in the composition of dietary supplements, and diphenyl diselenide (PhSe)2 is an important intermediate in organic synthesis, which increases the risk of human exposure to this chemical in the workplace. These compounds have been reported to inhibit the cerebral and hepatic aminolevulinic acid dehydratase (ALA-D) in vitro, and now we show that ascorbic acid can reverse some alterations caused by in vivo selenium exposure, but not ALA-D inhibition. The effect of Na2SeO3 or (PhSe)2 and ascorbic acid on selenium distribution, total non-protein thiol, ascorbic acid content (liver and brain) and haemoglobin was also examined. Mice were exposed to 250 micromol/kg (PhSe)2, or 18.75 micromol/kg Na2SeO3 subcutaneously, and to ascorbic acid, twice a day, 1 mmol/kg intraperitonially, for 10 days. Hepatic ALA-D of mice treated with (PhSe)2 was inhibited about 58% and similar results were observed in the animals that received ascorbic acid supplementation (P 0.10). Ascorbic acid treatment decreased significantly the hepatic and cerebral deposition of Se in (PhSe)2-exposed mice (P<0.01). Hepatic non-protein thiol content was not changed by treatment with (PhSe)2, ascorbic acid or (PhSe)2+ascorbic acid. Hepatic content of ascorbic acid was twice that in mice that received (PhSe)2, independent of ascorbic acid treatment (P<0.001). The results of this study suggest that vitamin C may have a protective role in organodiselenide intoxication.

https://onlinelibrary.wiley.com/doi/pdf/10.1034/j.1600-0773.2001.d01-92.x

Diphenyl diselenide and ascorbic acid changes deposition of selenium and ascorbic acid in liver and brain of mice

Publisher Summary This chapter discusses the environmental occurrence, health effects and management of lead poisoning. Lead poisoning is an old and a significant public-health problem throughout the world. Although the incidence of occupational and adult lead poisoning has declined in the recent past, the problem still exists. It often goes unrecognized for long periods because of the low index of suspicion compounded by incomplete surveillance of the risk population. Toxicity correlates with lead concentration in blood and progresses from biochemical and subclinical abnormalities, at levels around 10 μg/dL, to coma and to death at levels more than 100 μg/dL. Blood lead levels below 70 μg/dL can result in damage to the central nervous system, kidneys, and the hematopoietic system. Lead toxicity is also associated with a two to three point decrease in IQ test scores for every increase in 10 μg/dL in the lead level in blood. Elevated blood lead is also associated with neurodevelopment abnormalities—including attention-deficit disorders, behavioral disturbances, learning disabilities and deficits in fine and gross development.

Environmental occurrence, health effects and management of lead poisoning

Effect of organic forms of selenium on delta-aminolevulinate dehydratase from liver, kidney, and brain of adult rats.

Acetaminophen-induced liver damage in mice: Effects of some medicinal plants on the oxidative defense system

Effects of resveratrol on biomarkers of oxidative stress and on the activity of delta aminolevulinic acid dehydratase in liver and kidney of streptozotocin-induced diabetic rats

gamma-Aminolevulinic acid (ALA) dehydratase catalyzes the synthesis of porphobilinogen (PBG) from two molecules of ALA. A semimicro method for the colorimetric determination of ALA dehydratase is presented and applied to various tissues. The enzyme activity in adult male rat liver was 2.22 and 1.94 mumol PBG formed/g liver/h for homogenates assayed with or without dithiothreitol, respectively. The assay was linear for at least 2.5 h and for up to 2.5 mg tissue per assay. The Km for ALA was 4.0 X 10(-4)M and the pH optimum was 6.2-6.4. The effects of activators and inhibitors on enzyme activity are discussed.

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Papers

Delta-aminolevulinic acid dehydratase assay.