A dose-dependent effect of dimethyl sulfoxide on lipid content, cell viability and oxidative stress in 3T3-L1 adipocytes

Dludla, Phiwayinkosi V.; Jack, Babalwa; Viraragavan, Amsha; Pheiffer, Carmen; Johnson, Rabia; Louw, Johan; Muller, Christo J. F.

doi:10.1016/j.toxrep.2018.10.002

Cited by 75 publications

(70 citation statements)

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“…Remarkably, Raman spectrum in this study was decreasing of mitochondria associated peaks at 748 cm −1 and DNA/RNA bases associated peaks at 1657 cm −1 in Cd‐exposed sample (Figure and Table ). Furthermore, disturbing mitochondria function and excessive ROS leads to disordered internal environment in cells subsequently such as consumption of protein and loss of lipid . The Raman spectrum analysis in this study agreed with this tendency, Cd exposure decreased the protein and lipid related peaks (Table ), such as 1128, 1307 and 1585 cm −1 .…”

Section: Discussionsupporting

confidence: 85%

Ex vivo detection of cadmium‐induced renal damage by using confocal Raman spectroscopy

Shen

et al. 2019

Journal of Biophotonics

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Cadmium (Cd) is a toxic heavy metal which is harmful to environment and organisms. The reabsorption of Cd in kidney leads it to be the main damaged organ in animals under the Cd exposure. In this work, we applied confocal Raman spectroscopy to map the pathological changes in situ in normal and Cd‐exposed mice kidney. The renal tissue from Cd‐exposed group displayed a remarkable decreasing in the intensity of typical peaks related to mitochondria, DNA, proteins and lipids. On the contrary, the peaks of collagen in Cd‐exposed group elevated significantly. The components in each tissue were identified and distinguished by principal component analysis. Furthermore, all the biological investigations in this study were consistent with the Raman spectrum detection, which revealed the progression and degree of lesion induced by Cd. The confocal Raman spectroscopy provides a new perspective for in situ monitoring of substances changes in tissues, which exhibits more comprehensive understanding of the pathogenic mechanisms of heavy metals in molecular toxicology.

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Section: Discussionsupporting

confidence: 85%

Ex vivo detection of cadmium‐induced renal damage by using confocal Raman spectroscopy

Shen

et al. 2019

Journal of Biophotonics

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“…All compounds, including isoorientin and two positive controls of pioglitazone and CL-316,243, were prepared by diluting the appropriate amounts of a stock solution in phenol red free DMEM (supplemented with 8 mM glucose, 3.7 g/L NaHCO 3 , and 0.1% (w/v) bovine serum albumin (BSA)), to yield the final working concentrations. To eliminate interference of DMSO in the bioactivity of compounds, the final DMSO in all experiments was <0.001%, as previously reported [22]. Briefly, the treatment process involved a nutrient deprivation step where differentiated adipocytes were cultured in phenol red free DMEM, without glucose and serum (supplemented with 3.7 g/L NaHCO 3 , 0.1% (w/v) BSA), for 30 min prior to the addition of the relevant treatment.…”

Section: Preparation Of Compounds and Treatmentmentioning

confidence: 99%

Impact of Isoorientin on Metabolic Activity and Lipid Accumulation in Differentiated Adipocytes

et al. 2020

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The current study explored the effect of isoorientin on the metabolic activity and lipid accumulation in fully differentiated 3T3-L1 adipocytes. To achieve this, the 3T3-L1 pre-adipocytes were differentiated for eight days and treated with various concentrations of isoorientin (0.1–100 μM) for four hours. Subsequently, the metabolic activity, lipid accumulation, and mitochondrial respiration were assessed. Furthermore, to unravel the molecular mechanisms that might elucidate the bioactivity of isoorientin, protein expression of the genes involved in insulin signaling and energy expenditure, such as AKT and AMPK, were investigated. The results showed that isoorientin, at different doses, could block lipid storage and enhance glycerol release, with a concomitant improvement of the metabolic activity and mitochondrial function. Although the observed beneficial effects of isoorientin on these cultured 3T3-L1 adipocytes were not consistent at all concentrations, it was clear that doses between 1 and 10 μM were most effective compared to the untreated control. Moreover, the activity of isoorientin was comparable to tested positive controls of CL-316,2431, isoproterenol, insulin, and metformin. Mechanistically, protein expression of AKT and AMPK, was enhanced with isoorientin exposure, suggesting their partial role in modulating lipid metabolism and mitochondrial biogenesis. Indeed, our results showed that isoorientin has the ability to enhance mitochondrial respiration, as we observed an increase in the ATP and oxygen consumption rate. Therefore, we concluded that isoorientin has a potential to impact mitochondrial activity, lipid metabolism and energy expenditure using an in vitro experimental model of obesity.

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“…The analysis of the distribution allows the discrimination of the percentage of cell 7 debris (R-/Y-), live cells (R+/Y-) and dead cells (R+/Y+). On the other hand, a previously described method [23] making use of colorimetric measurement of the reduction of tetrazolium dye (MTT) to its insoluble formazan is a widely-used to measure metabolic activity of viable cells. Thereafter, absorbance was read at 570 nm using a…”

Section: Cell Viability and Metabolic Activity Assaysmentioning

confidence: 99%

Palmitate-induced toxicity is associated with impaired mitochondrial respiration and accelerated oxidative stress in cultured cardiomyocytes: the critical role of Coenzyme Q_9/10

Dludla

Silvestri

Orlando

et al. 2019

Preprint

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Impaired mitochondrial function concomitant to enhanced oxidative stress-induced damage are well established mechanisms involved in hyperlipidemia-induced cardiotoxicity. Coenzyme Q9/10 (CoQ) is known to be a critical component of the mitochondrial electron transport chain that efficiently supports the process of bioenergetics in addition to its antioxidant activities. However, there is very limited information on the direct effect of myocardial lipid overload on endogenous CoQ levels in association with mitochondrial respiration and oxidative stress status.Here, such effects were explored by exposing H9c2 cardiomyocytes to various doses (0.15 to 1 mM) of palmitate for 24 hours. The results demonstrated that palmitate doses ≥ 0.25 mM are enough to impair mitochondrial respiration and cause oxidative stress. Although endogenous CoQ levels are enhanced by palmitate doses ≤ 5 mM, this is not enough to counteract oxidative stress, but is sufficient to maintain cell viability of cardiomyocytes, suggesting a compensation mechanism. Palmitate doses > 5 mM caused severe mitochondrial toxicity, including reduction of cell viability. Interestingly, enhancement of CoQ levels with the lowest dose of palmitate (0.15 mM) was accompanied by a significantly reduction of CoQ oxidation status, as well as low cytosolic production of reactive oxygen species.From the overall findings, it appears that CoQ response may be crucial to improve mitochondrial function and thus protect against hyperlipidemia-induced insult. These results further suggest that therapeutic agents that can stimulate endogenous levels of CoQ may be beneficial in protecting the myocardium against diabetes associated complications.

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A dose-dependent effect of dimethyl sulfoxide on lipid content, cell viability and oxidative stress in 3T3-L1 adipocytes

Abstract: HighlightsDepending on the concentration, dimethyl sulfoxide (DMSO) can be toxic to cells.3T3-L1 adipocytes are a well-established model to study anti-obesity properties.DMSO doses ≥1% reduced cell viability and promoted cell damage in 3T3-L1 adipocytes.

Cited by 75 publications

References 25 publications

Ex vivo detection of cadmium‐induced renal damage by using confocal Raman spectroscopy

Ex vivo detection of cadmium‐induced renal damage by using confocal Raman spectroscopy

Impact of Isoorientin on Metabolic Activity and Lipid Accumulation in Differentiated Adipocytes

Palmitate-induced toxicity is associated with impaired mitochondrial respiration and accelerated oxidative stress in cultured cardiomyocytes: the critical role of Coenzyme Q_9/10

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A dose-dependent effect of dimethyl sulfoxide on lipid content, cell viability and oxidative stress in 3T3-L1 adipocytes

Abstract: HighlightsDepending on the concentration, dimethyl sulfoxide (DMSO) can be toxic to cells.3T3-L1 adipocytes are a well-established model to study anti-obesity properties.DMSO doses ≥1% reduced cell viability and promoted cell damage in 3T3-L1 adipocytes.

Cited by 75 publications

References 25 publications

Ex vivo detection of cadmium‐induced renal damage by using confocal Raman spectroscopy

Ex vivo detection of cadmium‐induced renal damage by using confocal Raman spectroscopy

Impact of Isoorientin on Metabolic Activity and Lipid Accumulation in Differentiated Adipocytes

Palmitate-induced toxicity is associated with impaired mitochondrial respiration and accelerated oxidative stress in cultured cardiomyocytes: the critical role of Coenzyme Q9/10

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Palmitate-induced toxicity is associated with impaired mitochondrial respiration and accelerated oxidative stress in cultured cardiomyocytes: the critical role of Coenzyme Q_9/10