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David C. Dorman - One of the best experts on this subject based on the ideXlab platform.
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Basal ganglia neurotransmitter concentrations in rhesus monkeys following subchronic Manganese Sulfate inhalation.
American Journal of Industrial Medicine, 2007Co-Authors: Melanie F. Struve, Brian E. Mcmanus, Brian A. Wong, David C. DormanAbstract:Background Manganese neurotoxicity in humans is recognized as a form of parkinsonism with lesions occurring predominantly within the globus pallidus, subthalamic nucleus, putamen, and caudate nucleus. Methods This study evaluated dopamine, 3,4-dihydroxyphenylacetic acid, homovanillic acid, serotonin, norepinephrine, 5-hydroxyindoleacetic acid, y-aminobutyric acid (GABA), and glutamate concentrations in the globus pallidus, caudate, and putamen of male rhesus monkeys exposed subchronically to either air or Manganese Sulfate (MnSO 4 ) at 0.06, 0.3, or 1.5 mg Mn/m 3 . Results An approximate 1.5-6-fold increase (vs. air-exposed controls) in mean brain Manganese concentration was observed following subchronic MnSO 4 exposure. A marginally significant (P
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tissue Manganese concentrations in young male rhesus monkeys following subchronic Manganese Sulfate inhalation
Toxicological Sciences, 2006Co-Authors: David C. Dorman, Melanie F. Struve, Carl U Parkinson, Marianne W Marshall, Arden R James, Brian A. WongAbstract:High-dose human exposure to Manganese results in Manganese accumulation in the basal ganglia and dopaminergic neuropathology. Occupational Manganese neurotoxicity is most frequently linked with Manganese oxide inhalation; however, exposure to other forms of Manganese may lead to higher body burdens. The objective of this study was to determine tissue Manganese concentrations in rhesus monkeys following subchronic (6 h/day, 5 days/week) Manganese Sulfate (MnSO4) inhalation. A group of monkeys were exposed to either air or MnSO4 (0.06, 0.3, or 1.5 mg Mn/m 3 ) for 65 exposure days before tissue analysis. Additional monkeys were exposed to MnSO4 at 1.5 mg Mn/m 3 for 15 or 33 exposure days and evaluated immediately thereafter or for 65 exposure days followed by a 45- or 90-day delay before evaluation. Tissue Manganese concentrations depended upon the aerosol concentration, exposure duration, and tissue. Monkeys exposed to MnSO4 at � 0.06 mg Mn/m 3 for 65 exposure days or to MnSO4 at 1.5 mg Mn/m 3 for � 15 exposure days developed increased Manganese concentrations in the olfactory epithelium, olfactory bulb, olfactory cortex, globus pallidus, putamen, and cerebellum. The olfactory epithelium, olfactory bulb, globus pallidus, caudate, putamen, pituitary gland, and bile developed the greatest relative increase in Manganese concentration following MnSO4 exposure. Tissue Manganese concentrations returned to levels observed in the air-exposed animals by 90 days after the end of the subchronic MnSO4 exposure. These results provide an improved understanding of MnSO4 exposure conditions that lead to increased concentrations of Manganese within the nonhuman primate brain and other tissues.
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nasal toxicity of Manganese Sulfate and Manganese phosphate in young male rats following subchronic 13 week inhalation exposure
Inhalation Toxicology, 2004Co-Authors: David C. Dorman, Brian E. Mcmanus, Carl U Parkinson, Chris A Manuel, Anna M Mcelveen, Jeffrey I EverittAbstract:Growing evidence suggests that nasal deposition and transport along the olfactory nerve represents a route by which inhaled Manganese and certain other metals are delivered to the rodent brain. The toxicological significance of olfactory transport of Manganese remains poorly defined. In rats, repeated intranasal instillation of Manganese chloride results in injury to the olfactory epithelium and neurotoxicity as evidenced by increased glial fibrillary acidic protein (GFAP) concentrations in olfactory bulb astrocytes. The purpose of the present study was to further characterize the nasal toxicity of Manganese Sulfate (MnSO4) and Manganese phosphate (as hureaulite) in young adult male rats following subchronic (90-day) exposure to air, MnSO4 (0.01, 0.1, and 0.5 mg Mn/m3), or hureaulite (0.1 mg Mn/m3). Nasal pathology, brain GFAP levels, and brain Manganese concentrations were assessed immediately following the end of the 90-day exposure and 45 days thereafter. Elevated end-of-exposure olfactory bulb, striat...
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nasal toxicity of Manganese Sulfate and Manganese phosphate in young male rats following subchronic 13 week inhalation exposure
Inhalation Toxicology, 2004Co-Authors: David C. Dorman, Brian E. Mcmanus, Carl U Parkinson, Chris A Manuel, Anna M Mcelveen, Jeffrey I EverittAbstract:Growing evidence suggests that nasal deposition and transport along the olfactory nerve represents a route by which inhaled Manganese and certain other metals are delivered to the rodent brain. The toxicological significance of olfactory transport of Manganese remains poorly defined. In rats, repeated intranasal instillation of Manganese chloride results in injury to the olfactory epithelium and neurotoxicity as evidenced by increased glial fibrillary acidic protein (GFAP) concentrations in olfactory bulb astrocytes. The purpose of the present study was to further characterize the nasal toxicity of Manganese Sulfate (MnSO(4)) and Manganese phosphate (as hureaulite) in young adult male rats following subchronic (90-day) exposure to air, MnSO(4) (0.01, 0.1, and 0.5 mg Mn/m(3)), or hureaulite (0.1 mg Mn/m(3)). Nasal pathology, brain GFAP levels, and brain Manganese concentrations were assessed immediately following the end of the 90-day exposure and 45 days thereafter. Elevated end-of-exposure olfactory bulb, striatum, and cerebellum Manganese concentrations were observed following MnSO(4) exposure to > or = 0.01, > or = 0.1, and 0.5 mg Mn/m(3), respectively. Exposure to MnSO(4) or hureaulite did not affect olfactory bulb, cerebellar, or striatal GFAP concentrations. Exposure to MnSO(4) (0.5 mg Mn/m(3)) was also associated with reversible inflammation within the nasal respiratory epithelium, while the olfactory epithelium was unaffected by Manganese inhalation. These results confirm that high-dose Manganese inhalation can result in nasal toxicity (irritation) and increased delivery of Manganese to the brain; however, we could not confirm that Manganese inhalation would result in altered brain GFAP concentrations.
Jeffrey I Everitt - One of the best experts on this subject based on the ideXlab platform.
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nasal toxicity of Manganese Sulfate and Manganese phosphate in young male rats following subchronic 13 week inhalation exposure
Inhalation Toxicology, 2004Co-Authors: David C. Dorman, Brian E. Mcmanus, Carl U Parkinson, Chris A Manuel, Anna M Mcelveen, Jeffrey I EverittAbstract:Growing evidence suggests that nasal deposition and transport along the olfactory nerve represents a route by which inhaled Manganese and certain other metals are delivered to the rodent brain. The toxicological significance of olfactory transport of Manganese remains poorly defined. In rats, repeated intranasal instillation of Manganese chloride results in injury to the olfactory epithelium and neurotoxicity as evidenced by increased glial fibrillary acidic protein (GFAP) concentrations in olfactory bulb astrocytes. The purpose of the present study was to further characterize the nasal toxicity of Manganese Sulfate (MnSO4) and Manganese phosphate (as hureaulite) in young adult male rats following subchronic (90-day) exposure to air, MnSO4 (0.01, 0.1, and 0.5 mg Mn/m3), or hureaulite (0.1 mg Mn/m3). Nasal pathology, brain GFAP levels, and brain Manganese concentrations were assessed immediately following the end of the 90-day exposure and 45 days thereafter. Elevated end-of-exposure olfactory bulb, striat...
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nasal toxicity of Manganese Sulfate and Manganese phosphate in young male rats following subchronic 13 week inhalation exposure
Inhalation Toxicology, 2004Co-Authors: David C. Dorman, Brian E. Mcmanus, Carl U Parkinson, Chris A Manuel, Anna M Mcelveen, Jeffrey I EverittAbstract:Growing evidence suggests that nasal deposition and transport along the olfactory nerve represents a route by which inhaled Manganese and certain other metals are delivered to the rodent brain. The toxicological significance of olfactory transport of Manganese remains poorly defined. In rats, repeated intranasal instillation of Manganese chloride results in injury to the olfactory epithelium and neurotoxicity as evidenced by increased glial fibrillary acidic protein (GFAP) concentrations in olfactory bulb astrocytes. The purpose of the present study was to further characterize the nasal toxicity of Manganese Sulfate (MnSO(4)) and Manganese phosphate (as hureaulite) in young adult male rats following subchronic (90-day) exposure to air, MnSO(4) (0.01, 0.1, and 0.5 mg Mn/m(3)), or hureaulite (0.1 mg Mn/m(3)). Nasal pathology, brain GFAP levels, and brain Manganese concentrations were assessed immediately following the end of the 90-day exposure and 45 days thereafter. Elevated end-of-exposure olfactory bulb, striatum, and cerebellum Manganese concentrations were observed following MnSO(4) exposure to > or = 0.01, > or = 0.1, and 0.5 mg Mn/m(3), respectively. Exposure to MnSO(4) or hureaulite did not affect olfactory bulb, cerebellar, or striatal GFAP concentrations. Exposure to MnSO(4) (0.5 mg Mn/m(3)) was also associated with reversible inflammation within the nasal respiratory epithelium, while the olfactory epithelium was unaffected by Manganese inhalation. These results confirm that high-dose Manganese inhalation can result in nasal toxicity (irritation) and increased delivery of Manganese to the brain; however, we could not confirm that Manganese inhalation would result in altered brain GFAP concentrations.
Carl U Parkinson - One of the best experts on this subject based on the ideXlab platform.
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tissue Manganese concentrations in young male rhesus monkeys following subchronic Manganese Sulfate inhalation
Toxicological Sciences, 2006Co-Authors: David C. Dorman, Melanie F. Struve, Carl U Parkinson, Marianne W Marshall, Arden R James, Brian A. WongAbstract:High-dose human exposure to Manganese results in Manganese accumulation in the basal ganglia and dopaminergic neuropathology. Occupational Manganese neurotoxicity is most frequently linked with Manganese oxide inhalation; however, exposure to other forms of Manganese may lead to higher body burdens. The objective of this study was to determine tissue Manganese concentrations in rhesus monkeys following subchronic (6 h/day, 5 days/week) Manganese Sulfate (MnSO4) inhalation. A group of monkeys were exposed to either air or MnSO4 (0.06, 0.3, or 1.5 mg Mn/m 3 ) for 65 exposure days before tissue analysis. Additional monkeys were exposed to MnSO4 at 1.5 mg Mn/m 3 for 15 or 33 exposure days and evaluated immediately thereafter or for 65 exposure days followed by a 45- or 90-day delay before evaluation. Tissue Manganese concentrations depended upon the aerosol concentration, exposure duration, and tissue. Monkeys exposed to MnSO4 at � 0.06 mg Mn/m 3 for 65 exposure days or to MnSO4 at 1.5 mg Mn/m 3 for � 15 exposure days developed increased Manganese concentrations in the olfactory epithelium, olfactory bulb, olfactory cortex, globus pallidus, putamen, and cerebellum. The olfactory epithelium, olfactory bulb, globus pallidus, caudate, putamen, pituitary gland, and bile developed the greatest relative increase in Manganese concentration following MnSO4 exposure. Tissue Manganese concentrations returned to levels observed in the air-exposed animals by 90 days after the end of the subchronic MnSO4 exposure. These results provide an improved understanding of MnSO4 exposure conditions that lead to increased concentrations of Manganese within the nonhuman primate brain and other tissues.
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nasal toxicity of Manganese Sulfate and Manganese phosphate in young male rats following subchronic 13 week inhalation exposure
Inhalation Toxicology, 2004Co-Authors: David C. Dorman, Brian E. Mcmanus, Carl U Parkinson, Chris A Manuel, Anna M Mcelveen, Jeffrey I EverittAbstract:Growing evidence suggests that nasal deposition and transport along the olfactory nerve represents a route by which inhaled Manganese and certain other metals are delivered to the rodent brain. The toxicological significance of olfactory transport of Manganese remains poorly defined. In rats, repeated intranasal instillation of Manganese chloride results in injury to the olfactory epithelium and neurotoxicity as evidenced by increased glial fibrillary acidic protein (GFAP) concentrations in olfactory bulb astrocytes. The purpose of the present study was to further characterize the nasal toxicity of Manganese Sulfate (MnSO4) and Manganese phosphate (as hureaulite) in young adult male rats following subchronic (90-day) exposure to air, MnSO4 (0.01, 0.1, and 0.5 mg Mn/m3), or hureaulite (0.1 mg Mn/m3). Nasal pathology, brain GFAP levels, and brain Manganese concentrations were assessed immediately following the end of the 90-day exposure and 45 days thereafter. Elevated end-of-exposure olfactory bulb, striat...
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nasal toxicity of Manganese Sulfate and Manganese phosphate in young male rats following subchronic 13 week inhalation exposure
Inhalation Toxicology, 2004Co-Authors: David C. Dorman, Brian E. Mcmanus, Carl U Parkinson, Chris A Manuel, Anna M Mcelveen, Jeffrey I EverittAbstract:Growing evidence suggests that nasal deposition and transport along the olfactory nerve represents a route by which inhaled Manganese and certain other metals are delivered to the rodent brain. The toxicological significance of olfactory transport of Manganese remains poorly defined. In rats, repeated intranasal instillation of Manganese chloride results in injury to the olfactory epithelium and neurotoxicity as evidenced by increased glial fibrillary acidic protein (GFAP) concentrations in olfactory bulb astrocytes. The purpose of the present study was to further characterize the nasal toxicity of Manganese Sulfate (MnSO(4)) and Manganese phosphate (as hureaulite) in young adult male rats following subchronic (90-day) exposure to air, MnSO(4) (0.01, 0.1, and 0.5 mg Mn/m(3)), or hureaulite (0.1 mg Mn/m(3)). Nasal pathology, brain GFAP levels, and brain Manganese concentrations were assessed immediately following the end of the 90-day exposure and 45 days thereafter. Elevated end-of-exposure olfactory bulb, striatum, and cerebellum Manganese concentrations were observed following MnSO(4) exposure to > or = 0.01, > or = 0.1, and 0.5 mg Mn/m(3), respectively. Exposure to MnSO(4) or hureaulite did not affect olfactory bulb, cerebellar, or striatal GFAP concentrations. Exposure to MnSO(4) (0.5 mg Mn/m(3)) was also associated with reversible inflammation within the nasal respiratory epithelium, while the olfactory epithelium was unaffected by Manganese inhalation. These results confirm that high-dose Manganese inhalation can result in nasal toxicity (irritation) and increased delivery of Manganese to the brain; however, we could not confirm that Manganese inhalation would result in altered brain GFAP concentrations.
Brian A. Wong - One of the best experts on this subject based on the ideXlab platform.
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Basal ganglia neurotransmitter concentrations in rhesus monkeys following subchronic Manganese Sulfate inhalation.
American Journal of Industrial Medicine, 2007Co-Authors: Melanie F. Struve, Brian E. Mcmanus, Brian A. Wong, David C. DormanAbstract:Background Manganese neurotoxicity in humans is recognized as a form of parkinsonism with lesions occurring predominantly within the globus pallidus, subthalamic nucleus, putamen, and caudate nucleus. Methods This study evaluated dopamine, 3,4-dihydroxyphenylacetic acid, homovanillic acid, serotonin, norepinephrine, 5-hydroxyindoleacetic acid, y-aminobutyric acid (GABA), and glutamate concentrations in the globus pallidus, caudate, and putamen of male rhesus monkeys exposed subchronically to either air or Manganese Sulfate (MnSO 4 ) at 0.06, 0.3, or 1.5 mg Mn/m 3 . Results An approximate 1.5-6-fold increase (vs. air-exposed controls) in mean brain Manganese concentration was observed following subchronic MnSO 4 exposure. A marginally significant (P
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tissue Manganese concentrations in young male rhesus monkeys following subchronic Manganese Sulfate inhalation
Toxicological Sciences, 2006Co-Authors: David C. Dorman, Melanie F. Struve, Carl U Parkinson, Marianne W Marshall, Arden R James, Brian A. WongAbstract:High-dose human exposure to Manganese results in Manganese accumulation in the basal ganglia and dopaminergic neuropathology. Occupational Manganese neurotoxicity is most frequently linked with Manganese oxide inhalation; however, exposure to other forms of Manganese may lead to higher body burdens. The objective of this study was to determine tissue Manganese concentrations in rhesus monkeys following subchronic (6 h/day, 5 days/week) Manganese Sulfate (MnSO4) inhalation. A group of monkeys were exposed to either air or MnSO4 (0.06, 0.3, or 1.5 mg Mn/m 3 ) for 65 exposure days before tissue analysis. Additional monkeys were exposed to MnSO4 at 1.5 mg Mn/m 3 for 15 or 33 exposure days and evaluated immediately thereafter or for 65 exposure days followed by a 45- or 90-day delay before evaluation. Tissue Manganese concentrations depended upon the aerosol concentration, exposure duration, and tissue. Monkeys exposed to MnSO4 at � 0.06 mg Mn/m 3 for 65 exposure days or to MnSO4 at 1.5 mg Mn/m 3 for � 15 exposure days developed increased Manganese concentrations in the olfactory epithelium, olfactory bulb, olfactory cortex, globus pallidus, putamen, and cerebellum. The olfactory epithelium, olfactory bulb, globus pallidus, caudate, putamen, pituitary gland, and bile developed the greatest relative increase in Manganese concentration following MnSO4 exposure. Tissue Manganese concentrations returned to levels observed in the air-exposed animals by 90 days after the end of the subchronic MnSO4 exposure. These results provide an improved understanding of MnSO4 exposure conditions that lead to increased concentrations of Manganese within the nonhuman primate brain and other tissues.
Brian E. Mcmanus - One of the best experts on this subject based on the ideXlab platform.
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Basal ganglia neurotransmitter concentrations in rhesus monkeys following subchronic Manganese Sulfate inhalation.
American Journal of Industrial Medicine, 2007Co-Authors: Melanie F. Struve, Brian E. Mcmanus, Brian A. Wong, David C. DormanAbstract:Background Manganese neurotoxicity in humans is recognized as a form of parkinsonism with lesions occurring predominantly within the globus pallidus, subthalamic nucleus, putamen, and caudate nucleus. Methods This study evaluated dopamine, 3,4-dihydroxyphenylacetic acid, homovanillic acid, serotonin, norepinephrine, 5-hydroxyindoleacetic acid, y-aminobutyric acid (GABA), and glutamate concentrations in the globus pallidus, caudate, and putamen of male rhesus monkeys exposed subchronically to either air or Manganese Sulfate (MnSO 4 ) at 0.06, 0.3, or 1.5 mg Mn/m 3 . Results An approximate 1.5-6-fold increase (vs. air-exposed controls) in mean brain Manganese concentration was observed following subchronic MnSO 4 exposure. A marginally significant (P
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nasal toxicity of Manganese Sulfate and Manganese phosphate in young male rats following subchronic 13 week inhalation exposure
Inhalation Toxicology, 2004Co-Authors: David C. Dorman, Brian E. Mcmanus, Carl U Parkinson, Chris A Manuel, Anna M Mcelveen, Jeffrey I EverittAbstract:Growing evidence suggests that nasal deposition and transport along the olfactory nerve represents a route by which inhaled Manganese and certain other metals are delivered to the rodent brain. The toxicological significance of olfactory transport of Manganese remains poorly defined. In rats, repeated intranasal instillation of Manganese chloride results in injury to the olfactory epithelium and neurotoxicity as evidenced by increased glial fibrillary acidic protein (GFAP) concentrations in olfactory bulb astrocytes. The purpose of the present study was to further characterize the nasal toxicity of Manganese Sulfate (MnSO4) and Manganese phosphate (as hureaulite) in young adult male rats following subchronic (90-day) exposure to air, MnSO4 (0.01, 0.1, and 0.5 mg Mn/m3), or hureaulite (0.1 mg Mn/m3). Nasal pathology, brain GFAP levels, and brain Manganese concentrations were assessed immediately following the end of the 90-day exposure and 45 days thereafter. Elevated end-of-exposure olfactory bulb, striat...
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nasal toxicity of Manganese Sulfate and Manganese phosphate in young male rats following subchronic 13 week inhalation exposure
Inhalation Toxicology, 2004Co-Authors: David C. Dorman, Brian E. Mcmanus, Carl U Parkinson, Chris A Manuel, Anna M Mcelveen, Jeffrey I EverittAbstract:Growing evidence suggests that nasal deposition and transport along the olfactory nerve represents a route by which inhaled Manganese and certain other metals are delivered to the rodent brain. The toxicological significance of olfactory transport of Manganese remains poorly defined. In rats, repeated intranasal instillation of Manganese chloride results in injury to the olfactory epithelium and neurotoxicity as evidenced by increased glial fibrillary acidic protein (GFAP) concentrations in olfactory bulb astrocytes. The purpose of the present study was to further characterize the nasal toxicity of Manganese Sulfate (MnSO(4)) and Manganese phosphate (as hureaulite) in young adult male rats following subchronic (90-day) exposure to air, MnSO(4) (0.01, 0.1, and 0.5 mg Mn/m(3)), or hureaulite (0.1 mg Mn/m(3)). Nasal pathology, brain GFAP levels, and brain Manganese concentrations were assessed immediately following the end of the 90-day exposure and 45 days thereafter. Elevated end-of-exposure olfactory bulb, striatum, and cerebellum Manganese concentrations were observed following MnSO(4) exposure to > or = 0.01, > or = 0.1, and 0.5 mg Mn/m(3), respectively. Exposure to MnSO(4) or hureaulite did not affect olfactory bulb, cerebellar, or striatal GFAP concentrations. Exposure to MnSO(4) (0.5 mg Mn/m(3)) was also associated with reversible inflammation within the nasal respiratory epithelium, while the olfactory epithelium was unaffected by Manganese inhalation. These results confirm that high-dose Manganese inhalation can result in nasal toxicity (irritation) and increased delivery of Manganese to the brain; however, we could not confirm that Manganese inhalation would result in altered brain GFAP concentrations.