Effectiveness of sodium 4,5-dihydroxybenzene-1,3-disulfonate (Tiron) in protecting against uranium-induced developmental toxicity in mice

Bosque, M. A.; Domingo, José L.; Llobet, Juan M.; Corbella, J.

doi:10.1016/0300-483x(93)90128-f

Cited by 28 publications

(15 citation statements)

References 20 publications

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“…Keeping this view in mind, some of the naturally occurring products having hydroxyl and/or carboxylic acid moiety may also be investigated besides synthetic chelators to attenuate beryllium poisoning. Tiferron, also known as tiron (sodium-4,5-dihydroxy-1,3-benzene disulphonate) is a catecholic compound and being a hydrophilic chelator, tried in treatment of a number of experimental metal toxicities including manganese [25], uranium [26], lead [27], vanadium [28] and beryllium [20,21]. a-Tocopherol is a chain breaking antioxidant that is known to protect biological membranes from oxidative damage [29,30], decreases thallium concentration in biological samples [31] and protects cell from copper and cadmium induced toxicity [32].…”

Section: Introductionmentioning

confidence: 99%

Amelioration of beryllium induced alterations in hepatorenal biochemistry and ultramorphology by co-administration of tiferron and adjuvants

et al. 2007

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Influence of adjuvants i.e., alpha-tocopherol (25 mg/kg, p.o.) and piperine (10 mg/kg, p.o.) on therapeutic potential of chelator tiferron (300 mg/kg, i.p.) was evaluated to encounter toxicogenic events of beryllium exposure. Albino rats were exposed to beryllium nitrate (1 mg/kg, i.p.) daily for 28 days followed by treatment of aforesaid therapeutic agents for 5 consecutive days. Results were considered to be significant at p < or =0.01 and p < or =0.05. Exposure to beryllium increased its concentration in liver, kidney and serum causing significant alterations in the activity of CYP-450 2E1 system, microsomal lipid peroxidation and protein; alkaline phosphtase, lactate dehydrogenase, gamma-glutamyl transpeptidase, bilirubin, creatinine and urea in serum; activity of acid phosphatase, alkaline phosphatase, adenosine triphosphatase, glucose-6-phosphatase and succinic dehydrogenase in liver and kidney. Beryllium exposure also induced severe alterations in histopathology and ultramorphology of liver and kidney proving its toxic consequences at cellular level. Tiferron along with adjuvants dramatically reversed alterations of all variables more towards control rather than individual treatment. Study concluded that tiferron in combination with alpha-tocopherol and piperine respectively was beneficial in diluting beryllium induced systemic toxicity; however, combination of tiferron and piperine presented more pronounced therapeutic potential.

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Section: Introductionmentioning

confidence: 99%

Amelioration of beryllium induced alterations in hepatorenal biochemistry and ultramorphology by co-administration of tiferron and adjuvants

et al. 2007

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“…The LD 50 of Tiron is significantly higher than that of other chelates. The NO-AEL (no-observable-adverse-effect level) for maternal and developmental toxicity of Tiron is 1500 mg/kg per day (Bosque et al 1993). The present study has clearly shown that Tiron is the effective chelator in the prevention of beryllium intoxication in pregnant rats and their fetuses.…”

Section: Discussionmentioning

confidence: 74%

Protective effect of Tiron (4,5-dihydroxybenzene-1,3-disulfonic acid disodium salt) against beryllium-induced maternal and fetal toxicity in rats

Sharma

Shah

Shukla

2002

Archives of Toxicology

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The efficacy of Tiron (4,5-dihydroxybenzene 1,3-disulfonic acid disodium salt) was examined in the treatment of beryllium-induced maternal and developmental toxicity in rats. Single administration of beryllium nitrate at a dose of 50 mg/kg (i.m.) on day 13 of gestation caused reductions in fetal and placental weights, the number of implantation sites and number of corpora lutea, as well as causing post-implantation loss, stunted growth, increase in the number of resorptions, and also a disturbed sex ratio. Maternal toxicity was demonstrated by reduction in body weight gain. Administration of beryllium also showed significant alteration in the hematological and biochemical indices of the mother as well as the fetus. Marked decreases were recorded in hemoglobin percentage, blood sugar levels, serum protein contents and serum alkaline phosphatase activity. By contrast, significant elevation was found in the activity of transaminases (aspartate aminotransferase and alanine aminotransferase). Tissue protein contents, glycogen contents, activities of alkaline phosphatase, adenosine triphosphatase and succinic dehydrogenase of kidney, lungs and uterus, and maternal and fetal liver all showed significantly decreased values after beryllium exposure, and remarkable elevation was observed in acid phosphatase, glucose-6-phosphatase and hepatic lipid peroxidation. These parameters were restored considerably with administration of 471 mg/kg i.m. Tiron from days 14 to 18 of gestation. Atomic absorption spectrophotometry also revealed a high concentration of beryllium in different organs of pregnant rats. Interestingly, a small amount of metal ion was also detected in the fetus and reduced accumulation of beryllium was noticed after Tiron treatment.

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“…These responses result in delayed growth, increased bone resorption rates, reduced bone volume and density, and increased fragility. Furthermore, evidence from various animal studies suggest that early life stages are susceptible to uranium-induced osteotoxicity (Bosque et al, 1992(Bosque et al, , 1993aDomingo et al, 1989;Pujadas Bigi et al, 2003;Pujadas Bigi and Ubios, 2007;Wade-Gueye et al, 2012).…”

Section: Discussionmentioning

confidence: 97%

“…A dose-dependent association between uranium exposure and altered development of the skeletal system, including unossified sternebrae and reduced ossification in caudal, parietal, occipital, carpal, vertebral, and metatarsal bones, was reported in various studies where Swiss albino mice exposed during gestation (Bosque et al, 1992(Bosque et al, , 1993aDomingo et al, 1989). The uraniuminduced alterations in fetal bone development were among the most sensitive developmental effects observed in the developing mouse fetus (Bosque et al, 1993b;Domingo et al, 1989).…”

Section: Uranium-induced Bone Toxicitymentioning

confidence: 92%

Modes of action associated with uranium induced adverse effects in bone function and development

2015

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Effectiveness of sodium 4,5-dihydroxybenzene-1,3-disulfonate (Tiron) in protecting against uranium-induced developmental toxicity in mice

Cited by 28 publications

References 20 publications

Amelioration of beryllium induced alterations in hepatorenal biochemistry and ultramorphology by co-administration of tiferron and adjuvants

Amelioration of beryllium induced alterations in hepatorenal biochemistry and ultramorphology by co-administration of tiferron and adjuvants

Protective effect of Tiron (4,5-dihydroxybenzene-1,3-disulfonic acid disodium salt) against beryllium-induced maternal and fetal toxicity in rats

Modes of action associated with uranium induced adverse effects in bone function and development

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