Lead oxalate (C2O4Pb) is an exogenous solid with an average molecular weight of 295.20 g/mol. Lead oxalate belongs to the dicarboxylic acids and derivatives, a subclass of carboxylic acids and derivatives within the organic compounds.
The compound interacts with 24 recorded protein targets. Lead binds to Acyl-CoA-binding protein (DBI), which regulates insulin secretion, steroidogenesis, intestinal cholecystokinin release, GABA-A/benzodiazepine receptor modulation, and acyl-CoA metabolism. It binds to an unnamed protein, thymosin beta-4, which acts as an immunotransmitter and functions in the stimulation of CaM-dependent kinases, GABA-A receptor complex function, and the modulation of cytoskeletion. Lead competitively inhibits the binding of calcium to calmodulin in another unnamed protein, causing improper activation that alters cAMP messenger pathways and interferes with neurotransmitter release. Competitive inhibition at the NMDA receptor, involving Glutamate receptor ionotropic NMDA 2A (GRIN2A), 2B (GRIN2B), 3A (GRIN3A), 3B (GRIN3B), and three other proteins, also affects neurotransmitter release.
Lead exhibits competitive inhibition with calcium at protein kinase C, involving Protein kinase C alpha type (PRKCA), beta type (PRKCB), delta type (PRKCD), epsilon type (PRKCE), and two other proteins, which alters the blood-brain barrier and impairs brain microvascular function and formation. Additionally, lead binds to sodium/potassium-transporting ATPases, including subunits alpha-1 (ATP1A1), alpha-2 (ATP1A2), alpha-3 (ATP1A3), gamma (FXYD2), and four other proteins. Finally, lead inhibits both Delta-aminolevulinic acid dehydratase (ALAD) and mitochondrial ferrochelatase (FECH), preventing the biosynthesis of heme, a necessary cofactor of hemoglobin.
belongs to the class of organic compounds known as dicarboxylic acids and derivatives. These are organic compounds containing exactly two carboxylic acid groups.
Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (8, 2, 3, 7)
Metabolism
Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (7)
Toxicity Values
Not Available
Lethal Dose
10 to 30 grams for and adult human (lead salts). (9)
Organic lead compounds are not classifiable as to their carcinogenicity to humans (Group 3). To the extent that organic lead compounds are metabolized in part to ionic lead, they are expected to exert the toxicities associated with inorganic lead (Group 2A, probably carcinogenic to humans). (6)
Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (4)
Symptoms
Symptions of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (1, 4)
Treatment
Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (4)
