RESUMEN
Sulfur mustard (SM) as an alkylating and vesicating agent was used for 100 years as a chemical weapon. SM as bi-functional mustard can attacks and alkylates lots of biomolecules. Different cellular mechanism and molecular pathways are responsible for damages to body tissues. Such as DNA damages, oxidative stress, Apoptosis, and inflammation. Sulfur mustard penetrated body organs and induces long term eye, skin, lung, gastrointestinal, urogenital damages and can cause carcinogenic and mutagenic consequences. Currently there is no definitive treatment protocol for SM exposed patients. The goal of treatment is relieving the symptoms with fast healing rate and retrieval of damaged tissues to normal function and appearance in short period of time. Evaluation of proteomics profile in SM-exposed victims has been performed in animal model and human patients. These studies revealed that different protein were involved in the patients with SM damages to skin and lungs. Apolipoprotein A1, type I cytokeratins K14, K16 and K17, S100 calcium-binding protein A8, α1 haptoglobin isoforms, Amyloid A1, albumin, haptoglobin, and keratin isoforms, immunoglobulin kappa chain are defined expressed proteins in the damaged tissues.
Asunto(s)
Gas Mostaza/toxicidad , Animales , Trastornos Químicamente Inducidos/diagnóstico , Trastornos Químicamente Inducidos/metabolismo , Trastornos Químicamente Inducidos/patología , Trastornos Químicamente Inducidos/terapia , Humanos , Masculino , ProteómicaAsunto(s)
Trastornos Químicamente Inducidos , Enfermedades Renales , Riñón/patología , Compuestos de Litio/toxicidad , Efectos Adversos a Largo Plazo , Trastornos Químicamente Inducidos/diagnóstico , Trastornos Químicamente Inducidos/etiología , Trastornos Químicamente Inducidos/patología , Diagnóstico Diferencial , Humanos , Enfermedades Renales/inducido químicamente , Enfermedades Renales/diagnóstico , Enfermedades Renales/patología , Compuestos de Litio/administración & dosificación , Efectos Adversos a Largo Plazo/inducido químicamente , Efectos Adversos a Largo Plazo/diagnóstico , Efectos Adversos a Largo Plazo/patología , Psicotrópicos/administración & dosificación , Psicotrópicos/toxicidadAsunto(s)
Trastornos Químicamente Inducidos , Indinavir/toxicidad , Enfermedades Renales , Riñón/patología , Efectos Adversos a Largo Plazo , Trastornos Químicamente Inducidos/diagnóstico , Trastornos Químicamente Inducidos/etiología , Trastornos Químicamente Inducidos/patología , Diagnóstico Diferencial , Inhibidores de la Proteasa del VIH/administración & dosificación , Inhibidores de la Proteasa del VIH/toxicidad , Humanos , Indinavir/administración & dosificación , Enfermedades Renales/inducido químicamente , Enfermedades Renales/diagnóstico , Enfermedades Renales/patología , Efectos Adversos a Largo Plazo/inducido químicamente , Efectos Adversos a Largo Plazo/diagnóstico , Efectos Adversos a Largo Plazo/patología , Factores de RiesgoRESUMEN
Pesticide formulation includes solvents (methanol and xylene) and antifreeze (ethylene glycol) whose metabolites are anions such as formic acid, hippuric acid, and oxalate. However, the effect of the anion gap on clinical outcome in acute pesticide intoxication requires clarification. In this prospective study, we compared the anion gap and other parameters between surviving versus deceased patients with acute pesticide intoxication. The following parameters were assessed in 1,058 patients with acute pesticide intoxication: blood chemistry (blood urea nitrogen, creatinine, glucose, lactic acid, liver enzymes, albumin, globulin, and urate), urinalysis (ketone bodies), arterial blood gas analysis, electrolytes (Na(+), K(+), Cl(-) HCO3 (-), Ca(++)), pesticide field of use, class, and ingestion amount, clinical outcome (death rate, length of hospital stay, length of intensive care unit stay, and seriousness of toxic symptoms), and the calculated anion gap. Among the 481 patients with a high anion gap, 52.2% had a blood pH in the physiologic range, 35.8% had metabolic acidosis, and 12.1% had acidemia. Age, anion gap, pesticide field of use, pesticide class, seriousness of symptoms (all P < 0.001), and time lag after ingestion (P = 0.048) were significant risk factors for death in univariate analyses. Among these, age, anion gap, and pesticide class were significant risk factors for death in a multiple logistic regression analysis (P < 0.001). In conclusions, high anion gap is a significant risk factor for death, regardless of the accompanying acid-base balance status in patients with acute pesticide intoxication.
Asunto(s)
Aniones/química , Biomarcadores/química , Plaguicidas/envenenamiento , Equilibrio Ácido-Base , Acidosis/etiología , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Aniones/metabolismo , Biomarcadores/metabolismo , Análisis de los Gases de la Sangre , Trastornos Químicamente Inducidos/mortalidad , Trastornos Químicamente Inducidos/patología , Electrólitos/análisis , Femenino , Humanos , Unidades de Cuidados Intensivos , Modelos Logísticos , Masculino , Persona de Mediana Edad , Oportunidad Relativa , Estudios Prospectivos , Factores de Riesgo , Análisis de Supervivencia , Urinálisis , Adulto JovenRESUMEN
Zearalenone (ZEA) is a mycotoxin commonly found as a contaminant in cereals. ZEA toxicity targets mainly the reproductive system, and oxidative stress plays an etiological role in its toxic effects. Therefore, the present study aimed to investigate the effect of lycopene, a potent carotenoid antioxidant, on markers of oxidative stress in liver, kidney and testes, and on reproductive, hematological and histopathological parameters after ZEA administration. Adult Swiss albino male mice received lycopene (20mg/kg, p.o.) for ten days before a single oral administration of ZEA (40mg/kg, p.o.), and 48h thereafter tissues (liver, kidney, testes and blood) were collected for biochemical, hematological and histological analyses. Lycopene prevented ZEA-induced changes in hematological parameters (increased number of leukocytes, segmented neutrophils, sticks, eosinophils and monocytes and decreased number of red blood cells (RBC), number of lymphocytes and platelets). Moreover, lycopene prevented the reduction in the number and motility of spermatozoa and the testicular tissue damage induced by ZEA. In addition, lycopene prevented the decrease in glutathione-S-transferase activity in kidney and testes and increased glutathione-S-transferase activity per se in the liver, kidneys and testes as well as superoxide dismutase activity in the liver. In summary, lycopene was able to prevent ZEA-induced acute toxic effects in male mice, suggesting that this antioxidant carotenoid may represent a promising prophylactic strategy against ZEA toxicity.