Biomedical subjects

J V Calderón-Salinas

Publications and source records attributed to J V Calderón-Salinas.

7 recordsLinked to original sources

PubMed2005

Effects of 1,25-dihydroxicolecalciferol and dietary calcium-phosphate on distribution of lead to tissues during growth.

The susceptibility to the toxic effects of lead (Pb) is mainly mediated by age and nutritional and hormonal status, and children are among the most vulnerable to them. During growth, an increase in calcium, phosphate and vitamin D in diet is recommended to enhance calcium and phosphate intestinal absorption and bone deposit. Calcium and phosphate reduce lead intestinal absorption, and 1,25-dihydroxicolecalciferol (1,25(OH)2D3) (active metabolite of vitamin D) increases both lead and calcium intestinal absorption. However, the effects of 1,25(OH)2D3 on lead bone deposit and redistribution to soft tissues are not well known. In this study, we examined the effects of calcium-phosphate diet supplementation and the administration of 1,25(OH)2D3 on Pb distribution to soft tissue and bone in growing rats exposed to Pb. Rats (21 days old) were exposed for 28 days to 100 ppm of Pb solution in drinking water. Calcium and phosphate in diet were increased from 1 to 2.5% and from 0.65 to 1.8%, respectively, and 1,25(OH)2D3 was administrated by intraperitoneal injection of 7.2 ng/kg every 7 days. Between 21 and 49 days, the body weight increased about 5 times. The results showed that high calcium-phosphate diet led to lower Pb concentration in blood and in bone, but Pb liver and kidney concentrations increased, which indicates that absorption and bone deposit redistribution of Pb decreased. On the other hand, no effect of this diet rich in calcium-phosphate in Pb concentration was observed in brain. Blood and bone Pb concentrations increased even more when the high calcium-phosphate diet included 1,25(OH)2D3. In the rats treated only with 1,25(OH)2D3, blood and bone Pb concentrations were lower. Higher concentrations of lead in the soft organs were observed also in rats treated under a high calcium-phosphate diet plus 1,25(OH)2D3 administration. The above mentioned results suggested that 1,25(OH)2D3 induces an increased absorption and redistribution of Pb, and therefore, it may enhance systemic damage in Pb-exposed growing animals.

Aging↗

PubMed2001

Cytochrome P450 2B (CYP2B)-mediated activation of methyl-parathion in rat brain extracts.

The role of cytochrome P450 (CYP) and the CYP isoform involved in the activation of the widely used pesticide methyl-parathion (MePA) were investigated in rat brain extracts by measuring the effect of different CYP inhibitors on acetylcholinesterase (AChE) inhibition by MePA. Brain extracts provide a useful tool to study the activation mechanisms of organophosphorus compounds (OP) since they contain both the activating enzyme(s) and the molecular target for OP toxicity. As expected, in incubations of rat brain extract supplemented with NADPH, AChE activity was non-competitively inhibited by the presence of MePA, indicating that MePA was activated to its reactive metabolite methyl-paraoxon (MePO). Indeed, Vmax(app) decreased from 13.4 to 8.7 micromol thionitrobenzoic acid (TNB)/min per mg protein. MePA activation by rat brain extracts, as measured by the AChE inhibition produced by the presence of the pesticide in the incubation, was fully prevented by previously bubbling the incubation mix with CO, by the presence of monoclonal anti-rat CYP2B1/2B2 antibodies and by the addition of phenobarbital (PB), a CYP2B substrate. Interestingly, MePA showed a greater affinity for CYP2B than PB. CYP1A1 antibodies showed no effect on MePA activation. The presence of cytochrome P450 2B (CYP2B) in the rat brain extracts was confirmed by immunoblotting. These results demonstrate indisputably the responsibility of CYP2B in MePA activation in the rat brain in vitro, suggesting that metabolic activation of OP compounds in situ might be crucial for their organ specific toxicity to the central nervous system also in vivo.

Acetylcholinesterase↗

PubMed1999

Effect of lead on the calcium transport in human erythrocyte.

In this paper we study the calcium uptake in the erythrocyte, a non-excitable cell. This uptake is performed through a passive transport system with two kinetic components (Michaelis-Menten and Hill). The uptake of calcium seems to be driven by voltage through its electrophoretical effect. Lead is capable of inhibiting calcium uptake in a non-competitive manner. As it has been described in other systems, lead is also capable of inhibiting calcium efflux by inhibiting Ca(Mg)-ATPase. Under physiological conditions, the function of ATPase reduces the effect of lead on calcium influx. However, in chronic intoxication a small increment of intracellular calcium is observed, indicating that lead is affecting calcium efflux mainly. We discuss the effects of lead on calcium equilibrium in erythrocytes.

Adult↗

PubMed1999

Lead and calcium transport in human erythrocyte.

In this paper we report the lead (Pb) and calcium (Ca) uptake by erythrocyte ghosts. In both cases the transport was carried out by a passive transport system with two kinetic components (Michaelis-Menten and Hill). Pb and Ca were capable of inhibiting the transport of the other metal in a non-competitive way. Under hyperpolarization, the uptakes of Ca and Pb were enhanced and the Michaelis-Menten component prevailed. Both Ca and Pb uptakes were inhibited by N-ethyl-maleimide to the same extent. These results indicate that Pb and Ca share the same permeability pathway in human erythrocytes and that this transport system is electrogenic.

Adult↗

PubMed1996

Lead exposure in a population of Mexican children.

The effects of low lead exposure were investigated in 96 children (7-12 years old) living and studying within a 1 km radius of a lead smelter (exposed population) located in Torreón, Coahuila, México, and compared with 30 children living and studying 4.5 km from the same smelter (control population). Both populations had similar socio-economic conditions. The exposed population showed higher blood lead (PbB) and free erythrocyte protoporphyrin (FEP) concentrations (17.3 +/- 5.6 micrograms dl-1 and 53.9 +/- 46.1 micrograms dl-1, respectively) than controls (PbB, 5.4 +/- 3.1 micrograms dl-1 and FEP, 13.9 +/- 7.3 micrograms dl-1). PbB concentrations were inversely correlated to distance from the smelter (r2 = 0.494). However, in the exposed population, wind direction also had a significant effect on the PbB and urinary lead (PbU) concentrations. The exposed population was divided according to PbB into a high level lead group (PbB > 15 micrograms dl-1), which also showed high FEP concentrations and a low lead group (PbB < 15 micrograms dl-1). Clinically, the high lead group showed a greater incidence of general symptoms (colic, headache, paresthesia, myalgia and dizziness), impairment of some neuromuscular functions (neuromuscular conduction velocity and motor coordination) and a decrease of intelligence quotient (IQ), which was not related with sex or socio-economic status. These results are an evidence of morbidity in children with high PbB concentrations.

Child↗

PubMed1996

Evolution of lead toxicity in a population of children.

A 3 years study was conducted to determine the evolution of blood lead concentrations (PbB) and free erythrocyte protoporphyrins (FEP) as indicators of absorption and biochemical damage in children (7-12 years old) living within one kilometer of a metallurgic factory that processes lead in Torreón, Coahuila, México. In addition, neuromuscular conduction velocity, motor coordination and IQ where determined as indicators of physiological damage. During this period of time the children showed increased lead blood concentrations of 19.2 +/- 4.5 micrograms dl-1 at the beginning of the study to 27.5 +/- 4.9 micrograms dl-1 at the end. Likewise, FEP increased from 56.6 +/- 20.0 micrograms dl-1 to 92.9 +/- 28.9 micrograms dl-1. Physiological damage was evident since motor coefficients as well as IQ tests were reduced significantly when compared to children (7-12 years old) living 4.5 km away from the factory who showed PbB = 8.9 +/- 1.3 micrograms dl-1 and FEP = 16.9 +/- 4.7 micrograms dl-1 throughout the study. Based on these data it was possible to define three different groups with regards to lead toxicity sensitivity.

Adult↗

PubMed1996

Lead: intestinal absorption and bone mobilization during lactation.

The aim of this study was to examine lead (Pb) intestinal absorption, its mobilization and redistribution during lactation in rats chronically exposed to lead. Lead and calcium (Ca) concentrations were measured in blood, milk, femurs, liver and kidney samples obtained from pregnant and lactating mother rats which were subjected to different schedules of exposure to Pb: 158 days before and during lactation (group A), 144 days before lactation (group B) and 14 days only during lactation (group C). Results were compared to those of non-pregnant but Pb-exposed matched rats and non-exposed control rats. In groups A and B during lactation, Pb in blood (PbB), liver and kidney increased while Pb in bone decreased. Since there was not an external source of Pb in group B during lactation, the results indicate resorption of Pb in bone as the main source of Pb in the organism. In group A, there was an additional increase of PbB when compared to group B as a result of Pb intestinal absorption. In group C a significant increase in PbB due to intestinal absorption and deposit in bone was found when compared to non-pregnant 144 days old rats, suggesting that the three processes intestinal absorption, bone resorption and bone absorption were taking place. These data indicate that Pb stored in bone as a result of prior maternal exposure, should be considered as a major source of self intoxication and of Pb in milk available to suckling pups.

Administration, Oral↗