Reproductive Biology and Toxicology Laboratory, School of Studies in Zoology, Jiwaji University, Gwalior (MP), India.
Therapie. 2012 Mar-Apr;67(2):173-82. doi: 10.2515/therapie/2012010. Epub 2012 Aug 2.
The aim of this study was to analyze the effect of tiferron (sodium 4, 5-dihydroxybenzene-1, 3-disulfonate) per se and combination with α-tocopherol against vanadium induced developmental toxicity. Vanadium, as vanadyl sulphate pentahydrate, was evaluated for embryotoxic/fetotoxic effect in female albino rats (Sprague Dawley).
The compound was administered by gavage to pregnant animals at a dose of 15 mg/kg/day, p.o. on day 6-15 of pregnancy (organogenesis). Tiferron was given on day 16-18 as chelating agent. Cesarean sections were performed on day 19 of gestation.
Maternal toxicity was observed, the level of sugar in the blood decreased, while we observed an increase in serum protein, serum alkaline phosphatase and serum transaminase activity. Level of lipid peroxidation showed enhances value in fetal and maternal liver. Vanadium induced inhibition in glycogen contents. Protein contents were decreased in vital organs where as increased in uterus and placenta. There was increased activity of acid phosphatase with the concomitant decline in alkaline phosphatase, adenosine triphosphatase and succnic dehydrogenase after vanadium intoxication. Toxicant caused severe alteration in histopathological observation of maternal and fetal liver, kidney, uterus and placenta proving its toxic consequences at cellular level. Tiferron along with α-tocopherol dramatically reversed alterations of all variables towards control rather than individual treatment.
The combination therapy of tiferron and α-tocopherol played a beneficial role in reducing vanadium induced developmental toxicity.
本研究旨在分析替非罗仑（4,5-二羟基苯-1,3-二磺酸钠）本身及其与α-生育酚联合应用对钒诱导的发育毒性的影响。以五水合硫酸氧钒的形式评估钒对雌性白化大鼠（Sprague Dawley）的胚胎毒性/胎儿毒性作用。
将该化合物通过灌胃给予怀孕动物，剂量为 15mg/kg/天，于妊娠第 6-15 天（器官发生期）口服。替非罗仑于第 16-18 天作为螯合剂给药。妊娠第 19 天进行剖宫产。
观察到母体毒性，血糖水平降低，而我们观察到血清蛋白、血清碱性磷酸酶和血清转氨酶活性增加。脂质过氧化水平显示胎肝和母肝的增强值。钒诱导肝糖原含量抑制。重要器官的蛋白质含量降低，而子宫和胎盘的蛋白质含量增加。酸性磷酸酶的活性增加，同时碱性磷酸酶、三磷酸腺苷酶和琥珀酸脱氢酶的活性下降，提示钒中毒后出现严重的变化。毒物对母胎肝、肾、子宫和胎盘的组织病理学观察造成严重改变，证明其在细胞水平上具有毒性后果。替非罗仑与α-生育酚联合治疗可显著逆转所有变量的改变，使其向对照而非单独治疗方向逆转。
替非罗仑和α-生育酚联合治疗在减轻钒诱导的发育毒性方面发挥了有益作用。
