ABSTRACT
Previous studies have suggested that arsenic crosses the placenta and affects the fetus development. The study under consideration aims to show comparative ameliorative effect of Moringa oleifera leaf and flower extracts against sodium arsenate induced fetus toxicity of mice. Pregnant mice (N=44) were kept in lab and divided into eleven group from (A to K) and were orally administered the doses 6 mg/kg, 12 mg/kg for sodium arsenate, 150 mg/kg and 300 mg/kg for Moringa oleifera leaf extracts (MOLE) and 150 mg/kg and 300 mg/kg for Moringa oleifera flower extracts (MOFE) comparing with control. The investigation revealed evident reduction in the fetuses weight, hind limb, fore limb, tail and snout length, crown rump and head circumferences well as malformations in tail, feet, arms, legs, skin and eyes in the negative control group (only administered with sodium arsenate). Co-administration of sodium arsenate with MOLE and MOFE ameliorate the reversed effect of sodium arsenate on the shape, length, body weight and DNA damage of fetus significantly at 95% confidence interval. However, Moringa oleifera leaf extract showed more significant results in comparison to Moringa oleifera flower extract. Hence concluded that Moringa oleifera leaf extract ameliorated the embryo toxic effects of sodium arsenate and can be used against environmental teratogens.
Estudos anteriores sugeriram que o arsênio atravessa a placenta e afeta o desenvolvimento do feto. O estudo em consideração visa mostrar o efeito melhorador comparativo de extratos de folhas e flores de Moringa oleifera contra a toxicidade fetal induzida por arseniato de sódio em camundongos. Camundongos grávidas (N = 44) foram mantidos em laboratório e divididos em 11 grupos (de A a K) e foram administrados por via oral nas doses de 6 mg/kg, 12 mg/kg para arseniato de sódio, 150 mg/kg e 300 mg/kg para extratos de folhas de Moringa oleifera (MOLE) e 150 mg/kg e 300 mg/kg para extratos de flores de Moringa oleifera (MOFE) em comparação com o controle. A investigação revelou redução evidente no peso do feto, membro posterior, membro anterior, comprimento da cauda e focinho, coroa, nádega e circunferência da cabeça, bem como malformações na cauda, pés, braços, pernas, pele e olhos no grupo de controle negativo (apenas administrado com arseniato de sódio). A coadministração de arseniato de sódio com MOLE e MOFE melhora significativamente o efeito reverso do arseniato de sódio na forma, comprimento, peso corporal e dano ao DNA do feto, com intervalo de confiança de 95%. No entanto, o extrato da folha da Moringa oleifera apresentou resultados mais significativos em comparação ao extrato da flor da Moringa oleifera. Portanto, concluiu que o extrato da folha de Moringa oleifera melhorou os efeitos tóxicos do arseniato de sódio para o embrião e pode ser usado contra teratógenos ambientais.
Subject(s)
Female , Animals , Pregnancy , Mice , Arsenates/toxicity , Comet Assay/veterinary , Fetus/abnormalities , Fetus/drug effects , Prenatal Injuries/veterinary , Moringa oleifera/embryologyABSTRACT
OBJECTIVES: To seek an interrelationship, if any, between oxidant stress and neurochemical changes in various rat brain regions after arsenic exposure. MATERIALS AND METHODS: This study was carried out at the Department of Biochemistry, Al Arab Medical University, Benghazi, Libya. Seventy five male Spraque-Dawley rats were divided into three groups: CONTROL GROUP: Rats were administered 2 ml of normal saline solution/kg body weight (b.wt.) daily for 20 days by intraperitoneal (i.p.) route. ARSENIC-TREATED GROUP: Rats received elemental arsenic (as sodium arsenate) 2.0 mg/kg b.wt. daily for 20 days by i.p. route. RECOVERY GROUP: Rats received 2.0 mg/kg b.wt. elemental arsenic daily for 20 days by i.p. route and were allowed to recover for 20 days. Rats were sacrificed and brains were dissected into cerebral cortex, corpus striatum, cerebellum and brain stem. Tissue homogenized in respective mediums. And were analyzed for lipid classes, oxidative stress, concentration of proteins, glutathione and ascorbic acid by utilizing standard colorimetric procedures. RESULTS: Arsenic exposure increased the oxidant stress because lipid peroxidation was enhanced. And decreased the contents of lipid classes, proteins, glutathione and the ascorbic acid in various rat brain regions. However, thins-layer chromatography exhibited regional variations in phospholipids classes. CONCLUSION: These results suggested that arsenic-initiated oxidant stress by increasing lipid peroxidation. The losses of lipid classes, ascorbic acid and glutathione may be attributed to peroxidative damage and binding of arsenic with sulfhydryl groups of enzymes. Recovery of animals showed reversibility in most of studied parameters, but gangliosides and cerebrosides over shooted. And speculated "Sphingolipidosis". It is then likely that repeated exposures of humans to arsenic may result in hampering of cell signalling, apoptosis and mutagenesis.
Subject(s)
Animals , Antioxidants/metabolism , Arsenates/toxicity , Ascorbic Acid/metabolism , Brain/metabolism , Chromatography, Thin Layer , Glutathione/metabolism , Lipid Peroxidation , Male , Oxidative Stress , Protein Biosynthesis/drug effects , Rats , Rats, Sprague-Dawley , Sphingolipidoses/chemically induced , Sulfhydryl Compounds/metabolismABSTRACT
Sodium arsenate (Na2HAsO4.7H2O) is a potent inhibitor of mungbean seed germination and seedling growth. Germination is totally stopped at or above 50 microM Na2HAsO4.7H2O. Inhibition of seedling elongation started at a lower concentration of 5 microM As(V) and was drastically reduced at 20 microM As(V). Nutrients like salts of macroelements viz., NaH2PO4.2H2O, KH2PO4, K2SO4, MgSO4.7H2O, CaCl2.2H2O, (NH4)2SO4 NH4NO3 solutions at a concentration of 10mM and microelements viz., ZnSO4, CuSO4.5H2O, Na2MoO4.2H2O, MnCl2.4H2O, CoCl2.6H2O, FeSO4.7H2O solutions at a concentration of 1mM could help to ameliorate the toxic effects of As(V) to different degrees. Amelioration of As(V) toxicity was possible only when the mungbean seeds were pretreated with the above mentioned nutrients for 24 hr and then transferred to sodium arsenate. Simultaneous treatment of nutrients with As(V) or using nutrient solutions following As(V) treatment were of no help to reverse the toxic effects of sodium arsenate.