Changes in Membrane Fluidity Induced by Tryptophan and its Metabolites

Rudzite, Vera; Jurika, Edite; Jirgensons, J.

doi:10.1007/978-1-4615-4709-9_46

Cited by 14 publications

(15 citation statements)

References 13 publications

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“…1) in CHO cells, whereas CrCl 3 treatments produced no decrease in cell survival over the same exposure times. The observed cytotoxicity of Pic is consistent with a previous report of increased S phase growth arrest in CHO cells with increasing time of exposure to picolinic acid [31]. However, in terms of DNA damage, Pic is less genotoxic than CrPic.…”

Section: Discussionsupporting

confidence: 93%

“…It is known to induce the expression of nitric oxide synthase and to act synergistically with interferon-c to activate macrophages [30]. Picolinic acid can also produce changes in cell membrane fluidity [31] and cell cycle arrest [32]. The toxicity of picolinic acid largely traces back to the observation that picolinic acid can chelate iron intracellularly [33] to produce reactive oxygen species through the Fenton mechanism [34].…”

Section: Discussionmentioning

confidence: 98%

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Ultrastructural damage in chromium picolinate-treated cells: a TEM study

2002

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Chromium picolinate (CrPic) is a human dietary supplement that provides a bioavailable form of chromium(III). Its mechanism of action is unknown, and a number of toxic endpoints have been attributed to its use. Understanding the cellular effects of CrPic is important for confirmation or dismissal of these potential toxic effects. The purpose of this work was to characterize morphological damage caused by CrPic, picolinic acid, and chromic chloride in Chinese hamster ovary AA8 cells. A 48-h exposure to 80 micro g/cm(2) CrPic (0.44 mg/mL CrPic) produced 45% survival by colony formation. Transmission electron microscopy (TEM) showed 83% of analyzed cells having swollen mitochondria with degraded cristae. Apoptosis was identified by nuclear convolution and fragmentation, and cytoplasmic blebbing. Apoptosis was quantified by fluorescence microscopy with acridine orange/ethidium bromide staining. At the 80 micro g/cm(2) dose of CrPic, 37% of the cells were apoptotic cells at 48 h. An equivalent dose of picolinate, 3 mM, was much more cytotoxic and thus there was an inadequate cell number for TEM analysis. However, a lower dose of 1.5 mM induced 49% cell survival, and damaged 86% of the mitochondria, with 51% of the cells undergoing apoptosis. A dose of 1 mM chromic chloride produced 71% cell survival, and damaged 86% of the mitochondria, with 22% of the cells undergoing apoptosis. The amount of apoptosis correlated with overall cell survival by colony formation, but not with the amount of mitochondrial damage. The coordination of Cr(III) by picolinate ligands may alter the cellular chemistry of Cr(III) to make chromium picolinate a toxic form of Cr(III).

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 98%

Ultrastructural damage in chromium picolinate-treated cells: a TEM study

2002

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“…We show here that BNA2-OE increases kynurenic acid, but how exactly this metabolite suppresses neutral lipid accumulation in aging cells remains to be determined. In this light, it is noteworthy that links have been described between kynurenine metabolites (e.g., kynurenic acid) and lipid metabolism in mammalian cells [32][33][34] . In particular, the regulation of IDO1 (the homolog of BNA2) activity and its expression is under complex regulation in metazoan cells [34][35][36][37] .…”

Section: Lipid Dropletsmentioning

confidence: 99%

Independent regulation of age associated fat accumulation and longevity

et al. 2020

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Age-dependent changes in metabolism can manifest as cellular lipid accumulation, but how this accumulation is regulated or impacts longevity is poorly understood. We find that Saccharomyces cerevisiae accumulate lipid droplets (LDs) during aging. We also find that overexpressing BNA2, the first Biosynthesis of NAD + (kynurenine) pathway gene, reduces LD accumulation during aging and extends lifespan. Mechanistically, this LD accumulation during aging is not linked to NAD + levels, but is anti-correlated with metabolites of the shikimate and aromatic amino acid biosynthesis (SA) pathways (upstream of BNA2), which produce tryptophan (the Bna2p substrate). We provide evidence that over-expressed BNA2 skews glycolytic flux from LDs towards the SA-BNA pathways, effectively reducing LDs. Importantly, we find that accumulation of LDs does not shorten lifespan, but does protect aged cells against stress. Our findings reveal how lipid accumulation impacts longevity, and how aging cell metabolism can be rewired to modulate lipid accumulation independently from longevity.

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“…The action of melatonin on the peroxidation of lipids in biological membranes has been studied in many laboratories [7,8], but to our knowledge only a few studies have shown how long chain PUFA such as C20:4 n-6, C22:5 n-3 and C22:6 n-3 are protected by this indole or its derivatives during the lipid peroxidation process [9][10][11]. In the present paper we report the ability of melatonin to protect against ascorbate-Fe ++ induced lipid peroxidation of rat liver, kidney and brain microsomes in vitro.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of melatonin on ascorbate‐Fe²⁺ lipid peroxidation of polyunsaturated fatty acids in rat liver, kidney and brain microsomes: a chemiluminescence study

Leaden

Catalá

2005

Journal of Pineal Research

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Melatonin (N-acetyl-5-methoxytryptamine), the main secretory product of the pineal gland, is a free radical scavenger that has been found to protect against lipid peroxidation in many experimental models. In the present study the effect of melatonin on lipid peroxidation of long chain polyunsaturated fatty acids located in rat liver, kidney and brain microsomes was determined using gas chromatography and a chemiluminescence assay. In vitro assays showed that after incubation of rat liver, kidney or brain microsomes in an ascorbate-Fe++ system, at 37 degrees C for 180 min, the total cpm originated from light emission (chemiluminescence) was found to be lower in those membranes incubated in the presence of melatonin. The incubation of rat liver, kidney or brain microsomes in the presence of ascorbate-Fe2+ resulted in lipid-peroxidation of membranes as evidenced by light emission and decrease of docosahexaenoic acid 22:6 n-3 and arachidonic acid 20:4 n-6. In the presence of melatonin (0.5, 1.0, 1.5 mm), light emission percent inhibition of microsomes was: (liver - 3.33, 9.98, 39.40) (kidney - 46.79, 61.88, 68.36) and (brain - 33.36, 28.89, 43.32). Not all fatty acids were equally protected after the addition of melatonin to the incubation medium. Our results indicate a selective protection of C20:4 n6 and C22:6 n3 by melatonin during non-enzymatic lipid peroxidation of rat liver, kidney and brain microsomes.

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Changes in Membrane Fluidity Induced by Tryptophan and its Metabolites

Cited by 14 publications

References 13 publications

Ultrastructural damage in chromium picolinate-treated cells: a TEM study

Ultrastructural damage in chromium picolinate-treated cells: a TEM study

Independent regulation of age associated fat accumulation and longevity

Protective effect of melatonin on ascorbate‐Fe²⁺ lipid peroxidation of polyunsaturated fatty acids in rat liver, kidney and brain microsomes: a chemiluminescence study

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Changes in Membrane Fluidity Induced by Tryptophan and its Metabolites

Cited by 14 publications

References 13 publications

Ultrastructural damage in chromium picolinate-treated cells: a TEM study

Ultrastructural damage in chromium picolinate-treated cells: a TEM study

Independent regulation of age associated fat accumulation and longevity

Protective effect of melatonin on ascorbate‐Fe2+ lipid peroxidation of polyunsaturated fatty acids in rat liver, kidney and brain microsomes: a chemiluminescence study

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Protective effect of melatonin on ascorbate‐Fe²⁺ lipid peroxidation of polyunsaturated fatty acids in rat liver, kidney and brain microsomes: a chemiluminescence study