Accumulation Of Lead In Blood Research Articles

Protective Effect of Porcine Cerebral Hydrolysate Peptides on Learning and Memory Deficits and Oxidative Stress in Lead-Exposed Mice.

In this study, lead acetate solution and porcine cerebral hydrolysate peptides (PCHPs) were administered to developing mice. Porcine cerebral protein pretreated by ultrasound was hydrolyzed with alcalase, and 11 peptide fragments were obtained by Matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) analysis of PCHPs. Our data showed that PCHPs significantly decreased Pb2+-induced spontaneous locomotor activity, latencies to reach the platform, and the time in target quadrant. It also decreased the accumulation of lead in the blood and brain of Pb2+-exposed developing mice. Co-administration of PCHPs and dimercaptosuccinic acid (DMSA) did not only reduce the accumulation of lead in blood but also increased the absorption of zinc and iron in Pb2+-exposed mice. Administration of PCHPs individually significantly enhanced hematopoietic parameters compared with the Pb2+-exposed group. PCHPs significantly reduced the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) but increased glutathione (GSH) content and anti-oxidant enzymes and nitric oxide synthase (NOS) activities in Pb2+-exposed brain. Our findings suggest that PCHPs have the ability to protect against Pb2+-exposed learning and memory deficits and oxidative damage.

Assessing Lead Effects on Fisher-344 Rats Using ICP-MS and Histology

Assessing Lead Effects on Fisher-344 Rats Using ICP-MS and Histology

Combined administration of a chelating agent and an antioxidant in the prevention and treatment of acute lead intoxication in rats

The administration of chelating agents, meso 2,3-dimercaptosuccinic acid (DMSA), monoisoamyl DMSA (MiADMSA) either individually or in combination with an antioxidant, n-acetylcysteine (NAC) in the prevention and treatment of acute lead intoxication in rats, was investigated. The results suggest that concomitant oral supplementation of DMSA with lead was most effective in preventing the inhibition of lead sensitive blood δ-aminolevulinic acid dehydratase (ALAD) activity in blood, elevation of zinc protoporphyrin level and the alterations in hepatic reduced and oxidized glutathione (GSH and GSSG) contents. A number of other biochemical variables either remained insensitive to lead exposure or responded moderately to chelation treatment. Combined administrations of NAC plus DMSA was most effective when given during lead exposure or post exposure, followed by DMSA and MiADMSA alone or NAC plus MiADMSA treatment, in reducing the accumulation of lead in blood and liver. Administration of NAC alone was only mildly effective in preventing lead absorption in the blood and tissues. The results suggest that combined administration of DMSA and NAC could be a more effective treatment protocol for acute lead toxicity, keeping in view its beneficial effect on oxidative injury.

Beneficial Effects of S-Adenosyl- l-Methionine on Aminolevulinic Acid Dehydratase, Glutathione, and Lipid Peroxidation During Acute Lead–Ethanol Administration in Mice

Beneficial effects of S-adenosyl- l-methionine (SAM) in preventing inhibition of blood delta-aminolevulinic acid dehydratase (ALAD), alterations in blood and hepatic glutathione (GSH), hepatic and brain malondialdehyde (MDA) formation, and uptake of lead following acute lead plus ethanol coexposure were investigated in mice. Whereas exposure to both lead or ethanol individually produced a significant inhibition of blood delta-aminolevulinic acid dehydratase (ALAD) activity, ethanol administration alone produced only a marginal depletion of hepatic glutathione (GSH). A significant elevation of hepatic MDA concentration was observed following lead or ethanol ingestion. An appreciable increase in brain GSH following ethanol administration whereas a moderate elevation in MDA level following lead plus ethanol administration was observed. Combined lead plus ethanol exposure produced a more pronounced depletion of blood ALAD activity and an increase in hepatic MDA level compared to lead- or ethanol-alone administration. Brain GSH concentration showed an increase compared to untreated control animals or lead-alone-exposed mice. Concomitant administration of SAM partially reversed the inhibition of blood ALAD activity in all three exposed groups (i.e., lead, ethanol, or lead plus ethanol). Lead concentration in blood, liver, and brain was significantly reduced by SAM in lead-alone or lead plus ethanol coexposed groups. The results suggest that supplementation of SAM may have beneficial effects in preventing alterations in some biochemical variables and accumulation of lead in blood, liver, and brain during acute lead plus ethanol exposure in animals.

Preventive Effects of Sodium Molybdate in Lead Intoxication in Rats

The role of sodium molybdate (1 mg/kg, intraperitoneally, once daily) supplementation during the course of lead exposure (0.1% lead acetate in drinking water for 4 weeks) in preventing the accumulation of lead in blood and soft tissues and in restoring altered lead-sensitive biochemical variables and the levels of hepatic glutathione, lipid peroxidation, blood Na, blood K, and serum ceruloplasmin was investigated in rats. The data indicate that sodium molybdate significantly protected the uptake of lead in blood, liver, and kidneys and restored the lead-induced inhibited activity of blood δ-aminolevulinic acid dehydratase, elevation of blood zinc protoporphyrin, hepatic lipid peroxidation, and serum ceruloplasmin. The results suggest a significant role of sodium molybdate in preventing plumbism.

Interaction of Zinc, Methionine or Their Combination with Lead at Gastrointestinal or Post‐Absorptive Level in Rats

The ability of zinc, methionine or their combination given by gavage to prevent or treat experimental oral lead intoxication in rats was investigated. Simultaneous oral supplementation with zinc plus methionine was found to be most effective in reducing lead induced inhibition of delta-aminolevulinic acid dehydratase (ALAD) activity in blood, elevation of urinary delta-aminolevulinic acid (ALA) excretion and in enhancing the hepatic glutathione (GSH) contents. The combination was also most effective in reducing the accumulation of lead in blood, liver and kidney compared to zinc or methionine alone. Prevention was more effective than treatment after lead exposure which may be caused by a decrease in the absorption of lead in the gastrointestinal tract in the presence of zinc and/or methionine.

Thiamine and zinc in prevention or therapy of lead intoxication.

Thiamine, zinc or their combination given through gastric gavage were investigated for their ability to prevent or treat experimental lead toxicity in rats. Simultaneous dietary supplementation with thiamine plus zinc was found to be the most effective way of reducing the lead-induced inhibition of delta-aminolevulinic acid dehydratase activity in blood, urinary, excretion of delta-aminolevulinic acid and accumulation of lead in blood, liver and kidney. Prevention was more effective than post-lead exposure treatment which may be due mainly to the decrease in the absorption of lead in the gastro-intestinal tract in the presence of thiamine and/or zinc.

Differential accumulation of lead by soft tissues of rabbit.

In studies on retention of lead by soft tissues, it is reported that, in acute and chronic intoxications, the concentration of Pb decrease in the following order: liver, kidney, heart and brain. The liver contains more lead than the other soft tissues; this might be due to the volume of blood that stays within the organ. Several parameters like age, temperature, perfusion, vascularity and residual blood volume could be important factors in the movement and differential accumulation of lead in blood and tissues. However, these parameters do not completely explain the quantitative differences in the retention of Pb between organs, and it is possible that other factors like the dose and the time between the administration of lead and the killing (exposure time), would have considerable importance in this process that so far has not been satisfactorily explained. The relationships between the size of a dose of lead given intravenously and the retention of this metal by some organs, as well as the effect of the duration of exposure of an intravenously administered dose of lead on accumulation were studied in this work. The possible relationships between accumulation and the values reported for perfusion and residual blood volumes were alsomore » studied.« less