In XRCC1 A399Q polymorphism,there were 0.37-fold and 0.52-fold decreased risk of lead poisoning in heterozygous mutation genotype(GA) and mutation genotype(GA+AA) compared with wild genotype(GG),respectively.
In XRCC1 A194W polymorphism,heterozygous mutation genotype (CT),homozygous mutation genotype(TT) and mutation genotype(CT+TT) could increase 2.03-fold,2.59-fold and 2.12-fold risk of lead poisoning compared with mild genotype(CC),respectively.
Many ocular manifestations of lead poisoning have been reported so far.
Stable isotope mass spectrometry in childhood lead poisoning
However, coexposure to lead and ethanol could result in more serious depletion of calcium and magnesium, and this could be the cause of suspected synergism between alcohol consumption and lead poisoning.
Alterations in the hepatic enzymes following experimental lead poisoning
Whereas significant inhibition of succinic dehydrogenase was seen following lead poisoning, the activity acid and alkaline phosphatase increased with lead intoxication.
Lead-exposed neonatal rats are frequently used as a model for plumbism in children.
Intravenous administration of 6 mg per kg lead acetate to rabbits resulted in plumbism with elevated erythrocyte lead levels and marked depression of activity of erythrocyte δ-aminolevulmic acid dehydratase.
The insensitivity of these erythrocyte enzymes to inhibition by lead excludes their usefulness for detection or diagnosis of plumbism.
In the in vitro inhibition test the same degree of inhibition of red cell P5N activity seen in hereditary red cell P5N deficiency was obtained by using a lead concentration 200-400 times higher than the lead levels detected in human plumbism.
Experimental plumbism in pigeons from the administration of metallic lead
In spite of the considerable achievements of the investigations of the different aspects of the saturnism problem, the question of an early diagnosis of the widely spread professional poisoning is not yet concluded.
It was established in chronic experiments on dogs that the picture of experimental lead poisoning was to a considerable extent similar to that seen during clinical manifestations of saturnism in human beings.
The autoxidation of d-aminolevulinic acid, in the presence or absence of oxyhemoglobin has been proposed as a source of oxy and carbon-centred radicals in the cells of intermittent acute porphyria and saturnism carriers.