Catecholamine contents of different region of adult rat brain are altered following short and long-term exposures to Pb[+2]

Catecholamine is a group of neurotransmitters that is believed to be responsible for the normal function of animal brain. Physiological and behavioral changes of human body have been reported due to the damage of the brain function following lead exposure. Due to the assumption of lead disposal in brain tissue with two year for its half-life, which results in alteration of brain function, we investigated the ability of lead to change the brain catecholamines during short and long-term studies. Rats were exposed daily with varying amounts of lead and catecholamine contents of cerebellum, mid-brain and brain cortex were determined. Acute peritoneal administration of single dose of lead as lead acetate [260 micro mol/Kg] after 2 h reduced [p < 0.05] the catecholamine levels of cerebellum, mid-brain and cortex part by 34.9%, 35.44% and 23.8%, respectively. The extension of experiment time to 5 h, significant [p < 0.05] reductions in catecholamine levels of mentioned regions of brain by 32.35%, 12.35% and 19.3% were seen respectively. Daily intraperitoneal administration of 10 micro mol/Kg lead for 30 and 60 days reduced catecholamines levels of cerebellum [22.22% and 30.44%], midbrain [12.48% and 26.27%] and brain cortex [11.58% and 26.7%] respectively. It might be concluded that brain dysfunction in lead intoxicated rat occurred through the reduction in the catecholamine levels of different parts of brain. Lead might be therefore considered as a probable factor in causing neurological disease in lead exposed man

El estres oxidativo como mecanismo de accion del plomo. Implicancias terapeuticas / Oxidative stress as a mechanism of action of lead. Therapeutic implications

El plomo (Pb) es un metal no esencial altamente toxico que afecta a diversos organos y tejidos. Si bien aun no ha sido descripto un mecanismo unico mediante el cual este metal ejerce sus efectos toxicos, un gran numero de estudios han puesto en evidencia el rol fundamental del estres oxidativo en la intoxicacion por Pb. A este respecto, ha sido informado que en la intoxicaci¨®n por Pb el estres oxidativo puede ocurrir a diferentes niveles: por generacion de acido ¦Ã-aminolevulinico (¦Ã-ALA), por la capacidad per se que posee el Pb para inducir peroxidacion lipidica en presencia de ion ferroso (Fe2+), o por deplecion de glutati¨®n (GSH) y enzimas antioxidantes. Sobre la base de estos antecedentes, el objetivo de esta revision es presentar evidencias recientes sobre la implicancia del estres oxidativo en los efectos adversos ocasionados por Pb, destacar la posibilidad de utilizacion de biomarcadores de estres oxidativo como un metodo complementario al diagnostico temprano de exposicion y revelar la importancia de los compuestos antioxidantes como nuevas herramientas en la prevencion y tratamiento de la intoxicacion por este metal.

Lead (Pb) is a highly toxic non-essential metal that affects different organs and tissues. Although at the present a unique mechanism by which this metal exerts its toxic effects has not been described, a large number of studies have highlighted the fundamental role of oxidative stress in the pathophysiology of Pb poisoning. In this regard, it has been reported that Pb-induced oxidative stress can occur at different levels: by the generation of ¦Ã-aminolevulinic acid (¦Ã-ALA), through its ability to induce lipid peroxidation in the presence of ferrous ion (Fe2+), or via glutathione (GSH) or antioxidant enzyme depletion. On the basis of these antecedents, the aim of this review is to present recent evidence regarding the implication of oxidative stress in the adverse effects caused by Pb, to emphasize the possibility to use oxidative stress biomarkers as a complementary method for early detection of Pb exposure, and to reveal the importance of antioxidant compounds as novel tools in the prevention and treatment of Pb exposure.

Oxidative stress in acute intermittent porphyria and lead poisoning may be triggered by 5-aminolevulinic acid

Highly reactive oxyradicals can be generated in vitro by iron-catalyzed aerobic oxidation of synthetic and naturally occuring substances capable of enolization in aqueous medium. Of biological interest are alfa-hydroxy- and alfa-aminocarbonyls such as carbohydrates, 5-aminolevulinic acid, and aminoacetone which tautomerize to the corresponding enediols and enolamines and yield oxyradicals initiated by electron transfer to dioxygen. Free radicals have been implicated in several normal and pathological processes. We briefly review our hypothesis of an in vivo prooxidant role of 5-aminolev-ulinic acid (ALA), the heme precursor accumulated in several porphyric disorders (e.g., lead poisoning, acute intermittent porphyria (AIP), tyrosinosis). Accordingly, i) ALA undergoes transition metal-catalyzed oxidation to give O-2, H2O2 and HO; ii) ALA induces iron release from ferritin, lipid peroxidation of cardiolipin-rich vesicles, single strand breaks in plasmid DNA, and guanosine oxidation in calf thymus DNA; iii) ALA causes Ca2+ -mediated rat liver mitochondria permeabilization; iv) rats chronically treated with ALA exhibit increased glycolytic metabolism; v) brain extracts of ALA-treated rats reveal increased levels of thiobarbituric acid reactive substances, direct chemiluminescence intensity, carbonyl proteins, ferritin, and "free iron"and gama-aminobutyric acid-receptor dissociation constant, and vi) patients with AIP and lead-exposed workers present augmented erythrocytic levels of the antioxidant enzymes superoxide dismutase and glutathione peroxidase. These data indicate the involvement of ALA-generated reactive species in the clinical manifestations (neuropathy, mental changes, muscle weakness, hepatoma) shared by the aforementioned inherited and acquired porphyric diseases.

Effects of chelation therapy on hepatic glutathione, lipid peroxidation and phospholipid contents in lead-poisoned rats.

Hepatic lipid peroxidation, glutathione and phospholipid contents of homogenate prepared from the liver of lead-intoxicated male rats treated with 0.3 m mol/kg CaNa2EDTA and DMSA for 8 weeks, either alone or in combination, were investigated. A significant increase in hepatic malondialdehyde (MDA) and a reduction in glutathione levels was noticed. While a marginal decrease in phosphatidyl choline (PC) level was noticed, no effect on phospholipid contents was seen. Treatment with all the three chelating agents elicited decrease in PC level. DMSA alone was partially effective in restoring lead-induced altered hepatic glutathione and MDA levels. Combined treatment may have an adverse effects on hepatic tissue and does not seem to produce immediate recoveries in the lead-induced hepatic damage.

Saturnismo: intoxicación por plomo / Saturnism: intoxication by plumb

El saturnismo es definido como la intoxicación aguda ó crónica por plomo o alguna de sus sales. Los autores hacen una amplia revisión sobre las características del plomo y sus componentes, su amplio uso en la industria y en infinidad de productos de uso en la vida diaria. Describen también su metabolismo y las alteraciones tóxicas que produce a nivel hematopeyético, sistema nervioso central, riñon y fibra muscular. Se revisa la clínica de esta entidad, en sus formas tanto crónica como aguda, y los métodos auxiliares de diagnóstico. Adicionalmente se revisan las bases del tratamiento actual y se, señalan pautas para la prevención de esta entidad en relación a trabajadores de plantas industriales, donde la incidencia es mayor.