Neurotoxicologic sequelae of tributyltin intoxication in rats

Elsabbagh, Hesham S.; moussa, Said.Z.; El-Tawil, Osama S.

doi:10.1006/phrs.2001.0909

Cited by 31 publications

(18 citation statements)

References 28 publications

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“…Acute exposure to TBT reduced the levels of DA, NE, and 5-HT in the whole brain of rats (Elsabbagh et al, 2002), as we found in this study of medaka. Tsunoda et al (2004) also reported that subacute exposure to TBT altered metabolism of DA in the midbrain of mice, which increased the HVA/ DA ratio.…”

Section: Discussionsupporting

confidence: 82%

“…In fish, serotonin (5-hydroxytryptamine) suppresses aggressive behavior (Adams et al, 1996), whereas dopamine (DA) stimulates such behavior (Munro, 1986;Tiersch and Griffith, 1988). In addition, TBT alters metabolism of DA in the midbrain of mice (Tsunoda et al, 2004) and reduces the concentrations of DA norepinephrine (NE), and serotonin in the whole brain of rats (Elsabbagh et al, 2002). Therefore, alteration of metabolism of brain monoamines might be a leading factor in behavioral impairments in medaka exposed to TBT.…”

Section: Introductionmentioning

confidence: 99%

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Alteration of monoamine concentrations in the brain of medaka, Oryzias latipes, exposed to tributyltin

Nakayama¹,

Oshima²,

Tachibana³

et al. 2007

Environmental Toxicology

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ABSTRACT:We measured the concentrations of monoamines in the brain of Japanese medaka, Oryzias latipes, exposed to tributyltin (TBT). Fish were exposed to 0, 1, 5, 25, or 125 g g À1 of TBT via the diet for 21 days. After the administration period, six males and six females in each treatment group were dissected and their brains were collected. The following monoamines were analyzed: dopamine (DA), norepinephrine (NE), epinephrine (E), and 5-hydroxytryptamine (5-HT). The metabolites of DA, 3,4-dihydroxyphenylacetic acid and homovanilic acid, and the metabolite of 5-HT, 5-hydroxyindolacetic acid were also analyzed. The concentration of DA in the brain of male medaka and the concentrations of 5-HT and NE in the female brains were significantly decreased by exposure to 125 g TBT g À1. The concentrations of 5-HT and NE in males and of DA in females were slightly decreased by 125 g g À1 of TBT, although the differences were not statistically significant. The present study demonstrates that TBT alters monoamine concentrations in the brain of medaka. # 2007 Wiley Periodicals, Inc. Environ Toxicol 22: 53-57, 2007.

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Section: Discussionsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Alteration of monoamine concentrations in the brain of medaka, Oryzias latipes, exposed to tributyltin

Nakayama¹,

Oshima²,

Tachibana³

et al. 2007

Environmental Toxicology

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“…The inhibition of this enzyme activity produces membrane depolarization, leading to the suppression of neuronal and excitatory transmission [19]. It is reported that organotins such as tributyltinoxide, trimethyltin, triethyltin and dibenzyltin suppress Na + /K + -ATPase activity in the brain [55,56]. Published studies showed that organotins affected the Na + /K + -ATPase activity and osmoregulation in European flounder, Platichthys flesus [57], through adjusting the Na + /K + flux.…”

Section: Discussionmentioning

confidence: 99%

Chronic Exposure to Tributyltin Induces Brain Functional Damage in Juvenile Common Carp (Cyprinus carpio)

Liu

Shi

2015

PLoS ONE

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The aim of the present study was to investigate the effect of Tributyltin (TBT) on brain function and neurotoxicity of freshwater teleost. The effects of long-term exposure to TBT on antioxidant related indices (MDA, malondialdehyde; SOD, superoxide dismutase; CAT, catalase; GR, glutathione reductase; GPx, glutathione peroxidase), Na+-K+-ATPase and neurological parameters (AChE, acetylcholinesterase; MAO, monoamine oxidase; NO, nitric oxide) in the brain of common carp were evaluated. Fish were exposed to sublethal concentrations of TBT (75 ng/L, 0.75 μg/L and 7.5 μg/L) for 15, 30, and 60 days. Based on the results, a low level and short-term TBT-induced stress could not induce the notable responses of the fish brain, but long-term exposure (more than 15 days) to TBT could lead to obvious physiological-biochemical responses (based on the measured parameters). The results also strongly indicated that neurotoxicity of TBT to fish. Thus, the measured physiological responses in fish brain could provide useful information to better understand the mechanisms of TBT-induced bio-toxicity.

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“…Interestingly, such an interaction might also explain why the m.9025G>A/p.MT-ATP6:G167S mutation, a candidate for the etiologic factor of a particular mitochondriopathy, is found in both patients and healthy individuals. The m.9025G>A mutation was found in a patient with loss of Purkinje cells (López-Gallardo et al 2014), and Purkinje cells showed degenerative changes throughout tributyltin-treated rat cerebellum (Elsabbagh et al 2002). …”

Section: Discussionmentioning

confidence: 99%

Effects of Tributyltin Chloride on Cybrids with or without an ATP Synthase Pathologic Mutation

López‐Gallardo

Llobet²,

Emperador³

et al. 2016

Environ Health Perspect

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Background:The oxidative phosphorylation system (OXPHOS) includes nuclear chromosome (nDNA)– and mitochondrial DNA (mtDNA)–encoded polypeptides. Many rare OXPHOS disorders, such as striatal necrosis syndromes, are caused by genetic mutations. Despite important advances in sequencing procedures, causative mutations remain undetected in some patients. It is possible that etiologic factors, such as environmental toxins, are the cause of these cases. Indeed, the inhibition of a particular enzyme by a poison could imitate the biochemical effects of pathological mutations in that enzyme. Moreover, environmental factors can modify the penetrance or expressivity of pathological mutations.Objectives:We studied the interaction between mitochondrially encoded ATP synthase 6 (p.MT-ATP6) subunit and an environmental exposure that may contribute phenotypic differences between healthy individuals and patients suffering from striatal necrosis syndromes or other mitochondriopathies.Methods:We analyzed the effects of the ATP synthase inhibitor tributyltin chloride (TBTC), a widely distributed environmental factor that contaminates human food and water, on transmitochondrial cell lines with or without an ATP synthase mutation that causes striatal necrosis syndrome. Doses were selected based on TBTC concentrations previously reported in human whole blood samples.Results:TBTC modified the phenotypic effects caused by a pathological mtDNA mutation. Interestingly, wild-type cells treated with this xenobiotic showed similar bioenergetics when compared with the untreated mutated cells.Conclusions:In addition to the known genetic causes, our findings suggest that environmental exposure to TBTC might contribute to the etiology of striatal necrosis syndromes.Citation:López-Gallardo E, Llobet L, Emperador S, Montoya J, Ruiz-Pesini E. 2016. Effects of tributyltin chloride on cybrids with or without an ATP synthase pathologic mutation. Environ Health Perspect 124:1399–1405; http://dx.doi.org/10.1289/EHP182

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Neurotoxicologic sequelae of tributyltin intoxication in rats

Cited by 31 publications

References 28 publications

Alteration of monoamine concentrations in the brain of medaka, Oryzias latipes, exposed to tributyltin

Alteration of monoamine concentrations in the brain of medaka, Oryzias latipes, exposed to tributyltin

Chronic Exposure to Tributyltin Induces Brain Functional Damage in Juvenile Common Carp (Cyprinus carpio)

Effects of Tributyltin Chloride on Cybrids with or without an ATP Synthase Pathologic Mutation

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