The autofluorescent products of lipid peroxidation may not be lipofuscin-like

Eldred, Graig E.; Katz, Martin I.

doi:10.1016/0891-5849(89)90007-5

Cited by 67 publications

(23 citation statements)

References 15 publications

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“…The results of these studies indicated that a blue fluorescent compound, possibly consisting of lipids, was the source of lipofuscin autofluorescence in tissues. However, it has also been shown that blue fluorescence can be induced artifactually through manipulations of the organic extract (e.g., light irradiation and chromatographic processes) (Eldred et al 1982;Eldred and Katz 1989;Kikugawa et al 1994). Recently, a series of reports has demonstrated that a lipofuscin-like compound is extractable by aqueous but not by organic solvents (Kikugawa et al 1994(Kikugawa et al ,1995(Kikugawa et al ,1997.…”

Section: Discussionmentioning

confidence: 99%

Reduction of Lipofuscin-like Autofluorescence in Fluorescently Labeled Tissue

Schnell

Staines

Wessendorf

1999

J Histochem Cytochem.

629

495

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SUMMARYThe fluorescent pigment lipofuscin accumulates with age in the cytoplasm of cells of the CNS. Because of its broad excitation and emission spectra, the presence of lipofuscin-like autofluorescence complicates the use of fluorescence microscopy (e.g., fluorescent retrograde tract tracing and fluorescence immunocytochemistry). In this study we examined several chemical treatments of tissue sections for their ability to reduce or eliminate lipofuscin-like autofluorescence without adversely affecting other fluorescent labels. We found that 1-10 mM CuSO 4 in 50 mM ammonium acetate buffer (pH 5) or 1% Sudan Black B (SB) in 70% ethanol reduced or eliminated lipofuscin autofluorescence in sections of monkey, human, or rat neural tissue. These treatments also slightly reduced the intensity of immunofluorescent labeling and fluorescent retrograde tract tracers. However, the reduction of these fluorophores was far less dramatic than that for the lipofuscin-like compound. We conclude that treatment of tissue with CuSO 4 or SB provides a reasonable compromise between reduction of lipofuscin-like fluorescence and maintenance of specific fluorescent labels.

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Section: Discussionmentioning

confidence: 99%

Reduction of Lipofuscin-like Autofluorescence in Fluorescently Labeled Tissue

Schnell

Staines

Wessendorf

1999

J Histochem Cytochem.

629

495

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“…When investigated further, however, this hypothesis could not be verified. The autofluorescent products of lipid oxidation were quite different from those seen in the lipofuscin granules of human RPE [31][32][33], and the vitamin E deficiency pigments of the RPE differed in solubility characteristics and fluorophoric composition from the age pigment granules [34], It has been argued that this long wavelength emission might be caused either by a concentrationdependent inner filter effect or by a metachromatic effect [35,36], In the case of RPE lipofuscin, this cannot be the case in that isolated diluted fluorophores still exhibit emission peaks ranging from yellow-green to orange-red in dilute solutions, consistent with the emissions from the in situ granules [37]. Fluorophores isolated from liver and heart age pigments also exhibited long-wavelength emissions, but differed from RPE fluorophores in their chromatographic mobilities [38].…”

Section: Accumulation Of Lipofuscin Granules In the Rpementioning

confidence: 94%

Lipofuscin Fluorophore Inhibits Lysosomal Protein Degradation and May Cause Early Stages of Macular Degeneration

Eldred

1995

Gerontology

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One of the autofiuorescent compounds that accumulates within the lipofuscin granules of the human retinal pigment epithelium (RPE) has now been identified as a quaternary nitrogen-containing cationic amphiphile (the bis-retinoid pyridinium salt, A2-E). Experimental evidence suggests that it may be responsible for lipofuscinogenesis in the RPE through its ability to inhibit lysosomal proteolysis. Furthermore, it may be involved in the events that trigger the changes leading to age-related macular degeneration (AMD), the leading cause of untreatable blindness in the elderly. It is suggested that if similar weakly basic nitrogenous compounds or cationic amphiphiles arise in reactions between amines and aldehydes in other tissues, a “self-assembling lysosomotropic amine” mechanism may provide an alternative explanation for lipofuscinogenesis those cell types as well.

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“…However, in studies on retinal pigment epithelium (RPE) lipofuscin, it was elucidated that oxidation products of neural retina and RPE-choroid homogenates from young rats produced autofluorescence, but corrected autofluorescence spectra of those products were different from that of RPE lipofuscin [34]. Furthermore, it was stated that RPE lipofuscin was a Schiff base reaction product of retinaldehyde and ethanolamine [35].…”

Section: Discussionmentioning

confidence: 99%

Formation of Lipofuscin-Like Autofluorescent Materials in NG108-15 Cells: Involvement of Lysosomal Protein Degradation

Mochizuki

Park²,

Mori³

et al. 1997

Gerontology

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We found that neuroblastoma × glioma hybrid NG108-15 cells accumulated lipofuscin-like autofluorescent materials during neuronal differentiation in culture in a medium containing 1% fetal calf serum, 1 mM dibutyryl cyclic AMP and 1 mM theophylline. The emission maximum of the lipofuscin-like autofluorescent materials was between 500 and 550 nm. Granules positive to acid phosphatase and periodic-acid Schiff were increased, as were the autofluorescent granules in NG108-15 cells. Thiolprotease inhibitors, N-(L-3-trans-carboxyoxirane-2-carbonyl)-L-leucine-4-aminobutylamide (E-64) and acetyl-Leu-Leu-Arg (leupeptin), markedly accelerated the accumulation of the lipofuscin-like autofluorescent materials in NG108-15 cells. On the other hand, activities of lysosomal thiolproteases, cathepsin B, C and L, were increased during neuronal differentiation. Protein content in the cells was gradually increased with the neuronal differentiation, and the rise was significantly accelerated when proteolysis was inhibited by E-64. These results suggest that the lipofuscin-like autofluorescent materials contain peptidic substances as a component, and indicate that the increase in hydrolytic activities of thiolproteases during neuronal differentiation is not enough for the hydrolysis of peptidic substrates, resulting in the accumulation of autofluorescent materials in NG108-15 cells.

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The autofluorescent products of lipid peroxidation may not be lipofuscin-like

Cited by 67 publications

References 15 publications

Reduction of Lipofuscin-like Autofluorescence in Fluorescently Labeled Tissue

Reduction of Lipofuscin-like Autofluorescence in Fluorescently Labeled Tissue

Lipofuscin Fluorophore Inhibits Lysosomal Protein Degradation and May Cause Early Stages of Macular Degeneration

Formation of Lipofuscin-Like Autofluorescent Materials in NG108-15 Cells: Involvement of Lysosomal Protein Degradation

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