Induction of Anti-Metallothionein Antibody and Mercury Treatment Decreases Bone Mineral Density in Mice

Jin, Guang‐Zhu

doi:10.1006/taap.2002.9531

Cited by 28 publications

(21 citation statements)

References 39 publications

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“…Conversely, MT mRNA expression significantly increased with both InHg and MeHg treatment. This result is similar to those from studies in mammals, as it has been demonstrated that MT plays a protective role in mercury-induced toxicity in bone (Jin et al, 2002). As it has been reported that osteoblasts express MT and protect from heavy metal (Angle et al, 1990;Nagata and Lönnerdal, 2011), the activation of MT in osteoblasts may be involved in resistance to mercury.…”

Section: Discussionsupporting

confidence: 90%

“…As it has been reported that osteoblasts express MT and protect from heavy metal (Angle et al, 1990;Nagata and Lönnerdal, 2011), the activation of MT in osteoblasts may be involved in resistance to mercury. In mammals, the influence of mercury on bone metabolism has been studied mainly by in vivo experiments and investigated in bone formation or osteoblastic activity (Yonaga et al, 1985;Jin et al, 2002). Both MeHg and InHg inhibited the growth of tibia in rats (Yonaga et al, 1985), and InHg decreased the serum levels of osteoblastic markers (ALP and osteocalcin) in rats (Jin et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…In mammals, the influence of mercury on bone metabolism has been studied mainly by in vivo experiments and investigated in bone formation or osteoblastic activity (Yonaga et al, 1985;Jin et al, 2002). Both MeHg and InHg inhibited the growth of tibia in rats (Yonaga et al, 1985), and InHg decreased the serum levels of osteoblastic markers (ALP and osteocalcin) in rats (Jin et al, 2002). Mammalian bone has resorptive cells (osteoclasts) and formative cells (osteoblasts).…”

Section: Discussionmentioning

confidence: 99%

“…To confirm the effects of InHg and MeHg on osteoclasts and osteoblasts, the mRNA expression of an osteoclast marker (tartrate-resistant acid phosphatase: TRAP) and an osteoblastic marker (collagen type I, α1: COL1A1) were partially sequenced and investigated using a quantitative PCR method. In addition, the mRNA expression of metallothionein (MT), which is a metalbinding protein that protects the organism from heavy metal (Hamer, 1986;Klaassen et al, 1999;Jin et al, 2002), was also examined.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Inorganic Mercury and Methylmercury on Osteoclasts and Osteoblasts in the Scales of the Marine Teleost as a Model System of Bone

et al. 2014

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To evaluate the effects of inorganic mercury (InHg) and methylmercury (MeHg) on bone metabolism in a marine teleost, the activity of tartrate-resistant acid phosphatase (TRAP) and alkaline phosphatase (ALP) as indicators of such activity in osteoclasts and osteoblasts, respectively, were examined in scales of nibbler fish (Girella punctata). We found several lines of scales with nearly the same TRAP and ALP activity levels. Using these scales, we evaluated the influence of InHg and MeHg. TRAP activity in the scales treated with InHg (10 -5 and 10 -4 M) and MeHg (10 -6 to 10 -4 M) during 6 hrs of incubation decreased significantly. In contrast, ALP activity decreased after exposure to InHg (10 -5 and 10 -4 M) and MeHg (10 -6 to 10 -4 M) for 18 and 36 hrs, although its activity did not change after 6 hrs of incubation. As in enzyme activity 6 hrs after incubation, mRNA expression of TRAP (osteoclastic marker) decreased significantly with InHg and MeHg treatment, while that of collagen (osteoblastic marker) did not change significantly. At 6 hrs after incubation, the mRNA expression of metallothionein, which is a metal-binding protein in osteoblasts, was significantly increased following treatment with InHg or MeHg, suggesting that it may be involved in the protection of osteoblasts against mercury exposure up to 6 hrs after incubation. To our knowledge, this is the first report of the effects of mercury on osteoclasts and osteoblasts using marine teleost scale as a model system of bone.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of Inorganic Mercury and Methylmercury on Osteoclasts and Osteoblasts in the Scales of the Marine Teleost as a Model System of Bone

et al. 2014

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“…Finally, in those severe lesions in which the meninges are disrupted, not only is there a strong reactive gliosis and cavitation, but also fibroblasts invade the lesion core and induce the astrocytic expression of particular guidance cues that are repulsive during development, such as Slit and ephrin-B2 as well as the ephrin receptors EphB2 and EphA4 (Turnley & Bartlett 1998;Bundesen et al 2003;Hagino et al 2003;Goldshmit et al 2004). The fibroblasts themselves express the repulsive guidance cue, Sema3 and axons attempting to regenerate express the Sema3 receptor, neuropilin, and are strongly repelled by the lesion core (Pasterkamp et al 1999;De Winter et al 2002;Jin et al 2002). So to encourage axons to grow through the glial scar, they must not only overcome inhibitory proteoglycans, which are expressed at all lesions, but also, depending on the severity of the lesion, ephrin-B2, Slit and Sema3.…”

Section: The Developmental Change In the Central Nervous System Envirmentioning

confidence: 99%

Recapitulate development to promote axonal regeneration: good or bad approach?

Filbin

2006

Phil. Trans. R. Soc. B

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In the past decade there has been an explosion in our understanding, at the molecular level, of why axons in the adult, mammalian central nervous system (CNS) do not spontaneously regenerate while their younger counterparts do. Now a number of inhibitors of axonal regeneration have been described, some of the receptors they interact with to transduce the inhibitory signal are known, as are some of the steps in the signal transduction pathway that is responsible for inhibition. In addition, developmental changes in the environment and in the neurons themselves are also now better understood. This knowledge in turn reveals novel, putative sites for drug development and therapeutic intervention after injury to the brain and spinal cord. The challenge now is to determine which of these putative treatments are the most effective and if they would be better applied in combination rather than alone. In this review I will summarize what we have learnt about these molecules and how they signal. Importantly, I will also describe approches that have been shown to block inhibitors and encourage regeneration in vivo. I will also speculate on what the differences are between the neonatal and adult CNS that allow the former to regenerate and the latter not to.

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Diphenyl diselenide protects against hematological and immunological alterations induced by mercury in mice

Brandão

Borges

Oliveira

et al. 2008

J Biochem & Molecular Tox

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Mercury is a heavy metal that can cause a variety of toxic effects on the organism, such as hematological and immunological alterations. In the present investigation, deleterious effects of mercury-intoxication in mice and a possible protective effect of diphenyl diselenide (PhSe)(2) were studied. Male adult Swiss albino mice received daily a pretreatment with (PhSe)(2) (15.6 mg/kg, orally) for 1 week. After this week, mice received daily mercuric chloride (1 mg/kg, subcutaneously) for 2 weeks. A number of hematological (erythrocytes, leukocytes, platelets, hemoglobin, hematocrit, reticulocytes, and leukocytes differential) and immunological (immunoglobulin G and M plasma concentration) parameters were evaluated. Another biomarker of tissue damage, lactate dehydrogenase (LDH), was also determined. The results demonstrated that mercury exposure caused a reduction in the erythrocyte, hematocrit, hemoglobin, leukocyte, and platelet counts and an increase in the reticulocyte percentages. (PhSe)(2) was effective in protecting against the reduction in hematocrit, hemoglobin, and leukocyte levels. (PhSe)(2) ameliorated reticulocyte percentages increased by mercury. However, (PhSe)(2) was partially effective in preventing against the decrease in erythrocyte and platelet counts. Immunoglobulin G and M concentrations and LDH activity were increased by mercury exposure, and (PhSe)(2) was effective in protecting against these effects. In conclusion, (PhSe)(2) was effective in protecting against hematological and immunological alterations induced by mercury in mice.

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Induction of Anti-Metallothionein Antibody and Mercury Treatment Decreases Bone Mineral Density in Mice

Cited by 28 publications

References 39 publications

Effects of Inorganic Mercury and Methylmercury on Osteoclasts and Osteoblasts in the Scales of the Marine Teleost as a Model System of Bone

Effects of Inorganic Mercury and Methylmercury on Osteoclasts and Osteoblasts in the Scales of the Marine Teleost as a Model System of Bone

Recapitulate development to promote axonal regeneration: good or bad approach?

Diphenyl diselenide protects against hematological and immunological alterations induced by mercury in mice

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