Lipid oxidation, lipoprotein cell-association and ceroid accumulation in P388D1 macrophage-like cells

Ce, Marchant; Ma, Bottoms; N, Law; Mitchinson, M. J.; Jv, Hunt

doi:10.1016/0005-2760(94)90052-3

Cited by 6 publications

(4 citation statements)

References 16 publications

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“…An elevation of fluorescence similar to FPLP frequently occurs in some aging or oxidatively stressed cells (9)(10)(11). This elevation is also associated with the appearanc< of yellow-fluorescence (520-540nm), which has a high resistance to oxidative stress (4)(5)(6), as well as with the effect of the yellow-fluorescent "inflammation" (namely, the increment of this intensity under the same conditions (12,13)).…”

Section: Introductionmentioning

confidence: 99%

On the Origin of Heterogeneity of Lipofuscin Fluorophores and Their Possible Interrelations

Schwartsburd¹

1995

Gerontology

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A comparision of the response of different cell types (thymus, spleen, liver, tumor) to the development of oxidative stress was investigated on an experimental model of tumor growth in vivo. Only spleen cells exhibited the yellow-red fluorescent pigment with high resistance to oxidative stress (as is typical for age-related lipofuscin pigment). Under oxidative stress, the cytoplasm in normal cells showed a tendency foward increased levels of fluorescent products of protein or lipid peroxidation, which was opposite from the response of tumor cells. In the present paper a novel hypothesis of lipofuscinogenesis is developed where oxidative stress is considered to be a trigger for switching on some adaptive cell pathways whose activity is associated with the induction of specific groups of cellular fluorophores.

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Section: Introductionmentioning

confidence: 99%

On the Origin of Heterogeneity of Lipofuscin Fluorophores and Their Possible Interrelations

Schwartsburd¹

1995

Gerontology

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“…11,17,[30][31][32][33] Ceroid is observed in various cell types and disease states and its formation has been linked to oxidative stress and pathological cellular senescence, commonly described as the aggregation of incomplete digestion products resulting from lysosomal and autophagosomal dysfunction. 24,34,35 Incubation of…”

Section: Discussionmentioning

confidence: 99%

“…11,17,30–33 Ceroid is observed in various cell types and disease states and its formation has been linked to oxidative stress and pathological cellular senescence, commonly described as the aggregation of incomplete digestion products resulting from lysosomal and autophagosomal dysfunction. 24,34,35 Incubation of cultured macrophages with oxLDL was reported to produce autofluorescence in the UV/visible range that could be inhibited with antioxidant treatment. 24,32,35 One study further demonstrated the potential for atheroma ceroid to possess a far-red fluorescence, with a tail into the NIR.…”

Section: Discussionmentioning

confidence: 99%

“…24,34,35 Incubation of cultured macrophages with oxLDL was reported to produce autofluorescence in the UV/visible range that could be inhibited with antioxidant treatment. 24,32,35 One study further demonstrated the potential for atheroma ceroid to possess a far-red fluorescence, with a tail into the NIR. 17 Importantly, it is well established that excessive accumulation of oxLDL triggers oxidative stress via dysfunction of cellular degradation machinery including the lysosome and endoplasmic reticulum that can be quenched with NAC.…”

Section: Discussionmentioning

confidence: 99%

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Near-Infrared Autofluorescence in Atherosclerosis Associates With Ceroid and Is Generated by Oxidized Lipid-Induced Oxidative Stress

Albaghdadi

Ikegami

Kassab

et al. 2021

ATVB

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Objective: Near-infrared autofluorescence (NIRAF) of atherosclerosis associates with intraplaque hemorrhage and is detectable in living patients with coronary artery disease. However, further mechanisms underlying NIRAF generation have not been fully characterized. Here, we investigated the role of lipids and oxidative stress in NIRAF generation in atherosclerosis and in vitro in human macrophages. Approach and Results: In N=15 human carotid endarterectomy specimens, we investigated the spatial distribution of lipid, intraplaque hemorrhage, and NIRAF (ex/em 630/650 nm). Plaque NIRAF associated with both Sudan black (SB)-positive lipids ( r =0.53, P =0.023) and GPA (glycophorin A)-positive intraplaque hemorrhage ( r =0.48, P =0.043). Plaque NIRAF also localized with lipid and specifically insoluble lipid (ceroid) and iron. Intriguingly, some NIRAF-positive areas were Sudan black-positive but GPA-negative. Studies on human macrophages investigated further the role of lipids in NIRAF generation. OxLDL (Oxidized low-density lipoprotein) and hemoglobin, but not LDL, generated NIRAF in both THP-1 cells and monocyte-derived macrophages. In oxLDL-treated THP-1 cells, higher NIRAF, lipid peroxidation products, and intracellular oxidative stress markers evolved ( P <0.001 versus LDL). The antioxidants α-tocopherol and N-acetylcysteine suppressed NIRAF generation and oxidative stress. Conclusions: In human atherosclerosis and human macrophages in vitro, NIRAF colocalizes with lipid and specifically insoluble lipid or ceroid. In vitro studies further show that oxidized LDL generates NIRAF, oxidative stress, and lipid peroxidation products. These results demonstrate a new pathway for NIRAF generation through oxidized lipid-driven oxidative stress and support ceroid as a source of NIRAF in human atherosclerosis. These findings may inform future clinical intracoronary NIRAF imaging studies of patients with coronary artery disease.

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Hypothesized molecular mechanism of formation of membrano-cystic lesions

Nakamura

2024

Medical Hypotheses

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Lipid oxidation, lipoprotein cell-association and ceroid accumulation in P388D1 macrophage-like cells

Cited by 6 publications

References 16 publications

On the Origin of Heterogeneity of Lipofuscin Fluorophores and Their Possible Interrelations

On the Origin of Heterogeneity of Lipofuscin Fluorophores and Their Possible Interrelations

Near-Infrared Autofluorescence in Atherosclerosis Associates With Ceroid and Is Generated by Oxidized Lipid-Induced Oxidative Stress

Hypothesized molecular mechanism of formation of membrano-cystic lesions

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