Adsorption of Mn(II) ions to human low density lipoproteins

Herak, Janko N.; Pifat, Greta; Brnjas-Krauević, Jasminka; Jürgens, Günther

doi:10.1016/0005-2760(82)90115-1

Cited by 7 publications

(1 citation statement)

References 21 publications

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“…If so, this suggests that the availability of blood manganese to the brain or the retention of manganese in the brain may differ depending in part on the oxidation state of manganese exposure. This suggestion is consistent with studies indicating that manganese normally exists in both Mn(II) and Mn(III) species within the blood (Hancock et al, 1973;Harris and Chen, 1994;Herak et al, 1982;Scheuhammer and Cherian, 1985) and with studies showing that Mn(II) and Mn(III) utilize different transport mechanisms for cellular uptake and transport across the blood-brain barrier; DMT-1 is known to transport Mn(II) species, and TfR-mediated endocytosis transports Mn(III)-transferrin species (Aschner and Gannon, 1993;Murphy et al, 1991;Zheng et al, 2003).…”

Section: Discussionsupporting

confidence: 89%

Brain Accumulation and Toxicity of Mn(II) and Mn(III) Exposures

Reaney¹,

Bench²,

Smith³

2006

Toxicological Sciences

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Concern over the neurotoxic effects of chronic moderate exposures to manganese has arisen due to increased awareness of occupational exposures and to the use of methylcyclopentadienyl manganese tricarbonyl, a manganese-containing gasoline antiknock additive. Little data exist on how the oxidation state of manganese exposure affects toxicity. The objective of this study was to better understand how the oxidation state of manganese exposure affects accumulation and subsequent toxicity of manganese. This study utilized a rat model of manganese neurotoxicity to investigate how ip exposure to Mn(II)-chloride or Mn(III)-pyrophosphate at total cumulative doses of 0, 30, or 90 mg Mn/kg body weight affected the brain region distribution and neurotoxicity of manganese. Results indicate that Mn(III) exposures produced significantly higher blood manganese levels than equimolar exposures to Mn(II). Brain manganese concentrations increased in a dose-dependent manner, with Mn(III) exposures producing significantly higher (> 25%) levels than exposures to Mn(II) but with no measurable differences in the accumulation of manganese across different brain regions. Gamma amino butyric acid concentrations were increased in the globus pallidus (GP) with manganese exposure. Dopamine (DA) levels were altered in the GP, with the highest Mn(II) and Mn(III) exposures producing significantly different DA levels. In addition, transferrin receptor and H-ferritin protein expression increased in the GP with manganese exposure. These data substantiate the heightened susceptibility of the GP to manganese, and they indicate that the oxidation state of manganese exposure may be an important determinant of tissue toxicodynamics and subsequent neurotoxicity.

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Section: Discussionsupporting

confidence: 89%

Brain Accumulation and Toxicity of Mn(II) and Mn(III) Exposures

Reaney¹,

Bench²,

Smith³

2006

Toxicological Sciences

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Surface-core correlations in serum lipoproteins

et al. 1984

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It has been found that the capacity of lipoproteins for binding Mn(II) ions is dependent on the arrangement of the lipoprotein core. A change in the molecular organization of the LDL core (thermotropic transition) is associated with the change on the lipoprotein surface. In HDL there is no thermotropic transition and no abrupt change of the binding capacity. The observed surface-core correlation might be an important link in understanding how dietary fat influences the lipoprotein metabolism.

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