Association between diphenyl diselenide and cadmium chloride attenuates the toxicity of both in tissues of mice in vitro

Brandão, Ricardo; Oliveira, Renata de; Nogueira, Cristina W.

doi:10.1016/j.tiv.2010.05.006

Cited by 7 publications

(7 citation statements)

References 35 publications

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“…(PhSe) 2 can prevent LPO induced by various prooxidants (Borges et al 2006;Brandão, de Oliveira, and Nogueira 2010;Rossato et al 2002). In this study, animals intoxicated with APAP had high levels of TBARS, indicating increased LPO.…”

Section: Discussionmentioning

confidence: 99%

“…administration in mice is 655 mg/kg (210 µmol/kg) (Nogueira, Meotti, et al 2003). In contrast, high doses of (PhSe) 2 inhibit δ-ALA-D activity in vitro in human blood (Nogueira, Borges, et al 2003) and cerebral Na + , K + -ATPase activity (Borges, Rocha, and Nogueira 2005) by interacting with the SH groups of these enzymes (Brandão, de Oliveira, and Nogueira 2010). However, studies have shown that (PhSe) 2 at a low concentration does not have a toxic effect (Rosa et al 2007; Straliotto et al 2010).…”

Section: Introductionmentioning

confidence: 99%

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Reduction of Acute Hepatic Damage Induced by Acetaminophen after Treatment with Diphenyl Diselenide in Mice

et al. 2012

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In this study, the authors evaluated the ability of diphenyl diselenide (PhSe) 2 to reverse acute hepatic failure induced by acetaminophen (APAP) in mice. The animals received an APAP dose of 600 mg/kg intraperitoneally (i.p.), and then 1 hour later, they received 15.6 mg/kg i.p. of (PhSe) 2 . Three hours after (PhSe) 2 administration, the animals were sacrificed and blood and liver samples were collected for analysis. The serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured. The levels of reduced glutathione (GSH) and oxidized glutathione (GSSG), thiobarbituric acid-reactive substances (TBARS), 2',7'-dichlorofluorescein (DFC), catalase activity (CAT), and myeloperoxidase (MPO) activity were determined in the liver. A methyl-tetrazolium reduction (MTT) assay was also performed on the liver. Histopathological studies were conducted in all groups. Exposure of animals to APAP induced oxidative stress, increased lipid peroxidation (LPO), and the generation of reactive species, reduced the levels of GSH, and caused an increase in the MPO activity. Treatment with (PhSe) 2 reduced LPO and the formation of reactive species and inhibited the processes of inflammation, reducing the hepatic damage induced by APAP. The results of this study show that (PhSe) 2 is a promising therapeutic option for the treatment of acute hepatic failure.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Reduction of Acute Hepatic Damage Induced by Acetaminophen after Treatment with Diphenyl Diselenide in Mice

et al. 2012

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“…Taking into account that δ‐ALA‐D is a metalloenzyme that requires zinc ions for its activity (Jaffe et al ., ), this enzyme could be inhibited by substances that compete with zinc and/or oxidize the –SH groups (Brandão et al ., ; Farina et al ., ; Nogueira et al ., ) and it is linked to situations associated with oxidative stress (Tandon et al ., ). Numerous metals such as mercury (Peixoto et al ., ), lead (Wang et al ., ), Cd (Brandão et al ., , ; Luchese et al ., ; Santos et al ., ,, ) and other compounds that oxidize sulfhydryl groups can modify the enzyme activity (Flora et al ., ; Wang and Fowler, ). In this way, δ‐ALA‐D activity could be used as a marker of metal toxicity.…”

Section: Introductionmentioning

confidence: 99%

“…d-Aminolevulinate dehydratase (d-ALA-D), a sulfhydryl enzyme, catalyzes the asymmetric condensation of two molecules of d-aminolevulinic acid (d-ALA) to porphobilinogen in the initial steps of heme biosynthesis (Gibson et al, 1955). Taking into account that d-ALA-D is a metalloenzyme that requires zinc ions for its activity (Jaffe et al, 1995), this enzyme could be inhibited by substances that compete with zinc and/or oxidize the -SH groups (Brandão et al, 2010;Farina et al, 2001;Nogueira et al, 2003a) and it is linked to situations associated with oxidative stress (Tandon et al, 2002). Numerous metals such as mercury (Peixoto et al, 2007), lead (Wang et al, 2011), Cd (Brandão et al, 2009(Brandão et al, , 2010Luchese et al, 2007;Santos et al, 2005aSantos et al, ,b, 2006 (Flora et al, 2002;Wang and Fowler, 2008).…”

Section: Introductionmentioning

confidence: 99%

Cadmium inhibits the ovary δ‐aminolevulinate dehydratase activity in vitro and ex vivo: protective role of seleno‐furanoside

Vargas

Soares

Izaguirry

et al. 2012

J of Applied Toxicology

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Cadmium (Cd) toxicity is a concern to the tobacco-smoking sub-population which includes millions of people worldwide. Although this metal may cause severe damage to embryos and the reproductive organs, the precise mechanisms underlying its toxicity remain unclear. In the present study, the Cd effect on ovary δ-aminolevulinate dehydratase (δ-ALA-D) activity was investigated in vitro and ex vivo. We observed that low concentrations of Cd inhibited cow ovary δ-ALA-D activity in vitro and the IC50 value obtained was 19.17 μM. Furthermore, the protective effect of a novel organic selenium compound (seleno-furanoside) in restoring enzyme activity was evaluated. Seleno-furanoside (10, 50, 100, 200, 400 and 1000 μM) did not reverse the Cd toxicity in bovine ovarian tissue in vitro. According to the in vitro reults, acute Cd exposure (2.5 and 5 mg kg(-1)) caused a significant inhibition in ovary δ-ALA-D activity in mice (around 27% and 34%, respectively). Therapy with seleno-furanoside (100 µmol kg(-1)) was able to restore enzyme activity. Thus, we demonstrated for the first time that δ-ALA-D activity from ovary is inhibited by Cd both in vitro and ex vivo. Additionally, seleno-furanoside therapy was effective in restoring ovarian enzyme activity inhibited by Cd exposure in mice, but it did not reverse the in vitro metal effect. This study detected a new toxicity marker of Cd toxicity on ovarian tissue as well as the beneficial effect of a new compound to manage the metal effect after acute exposure.

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“…catalase and hemoglobin) consisting of a protoporphyrin ring and a central iron (Fe) atom. Interestingly, δ ‐ALA‐D activity has been found to be inhibited in other experimental models of renal toxicity (Corte et al ., ; Brandão et al ., ) and in patients with chronic renal failure (Da Silva et al ., ). The analyses of the results suggest that administration of BPD to rats for 6 days was effective in mitigating harmful effects of cisplatin on δ ‐ALA‐D activity.…”

Section: Discussionmentioning

confidence: 99%

(E)‐2‐Benzylidene‐4‐phenyl‐1,3‐diselenole ameliorates signals of renal injury induced by cisplatin in rats

Bortolatto

Wilhelm

Roman

et al. 2012

J of Applied Toxicology

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The present study investigated the protective role of antioxidant (E)-2-benzylidene-4-phenyl-1,3-diselenole (BPD), an organoselenium compound, against the renal injury induced by cisplatin in rats. Canola oil or BPD (50 mg kg(-1)) was administered orally by gavage once a day for 6 days to rats. The first dose of BPD was given 24 h before a single intraperitoneal injection of saline or cisplatin (7 mg kg(-1)). At day 7, animals were killed and parameters related to renal injury were determined. The histological analysis showed that cisplatin caused renal injury in rats, which was accompanied by an increase in urea and creatinine levels in plasma. The increase of plasma creatinine levels negatively correlated with renal antioxidant defenses including ascorbic acid (AA) and reduced glutathione (GSH) content as well as glutathione S-transferase (GST), glutathione peroxidase (GPx) and catalase (CAT) activities. As revealed by histological analysis, BPD ameliorated tubular injury in rat kidney and reduced plasma markers altered by cisplatin. The administration of BPD to rats attenuated the reduction of renal AA and GSH content in animals exposed to cisplatin. The decrease of GST activity, but not GPx and CAT activities, in rats exposed to cisplatin was totally reversed by BPD administration. BPD was also effective in attenuating the inhibition of a sulfhydryl enzyme sensitive to oxidative stress, δ-aminolevulinic dehydratase, in kidneys of rats exposed to cisplatin. The present study demonstrated that BPD reduced renal injury induced by cisplatin in rats and this effect seems to be related to antioxidant mechanisms.

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Association between diphenyl diselenide and cadmium chloride attenuates the toxicity of both in tissues of mice in vitro

Cited by 7 publications

References 35 publications

Reduction of Acute Hepatic Damage Induced by Acetaminophen after Treatment with Diphenyl Diselenide in Mice

Reduction of Acute Hepatic Damage Induced by Acetaminophen after Treatment with Diphenyl Diselenide in Mice

Cadmium inhibits the ovary δ‐aminolevulinate dehydratase activity in vitro and ex vivo: protective role of seleno‐furanoside

(E)‐2‐Benzylidene‐4‐phenyl‐1,3‐diselenole ameliorates signals of renal injury induced by cisplatin in rats

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