Dimethyl sulphoxide dose–response on rat retinal function

Tsai, Tina I.; Bui, Bang V.; Vingrys, Algis J.

doi:10.1007/s10633-009-9191-8

Cited by 22 publications

(20 citation statements)

References 42 publications

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“…5, DMSO‐induced cell death increased expression of Bax in mitochondrial extracts at final concentrations of 2 and 4 but not 1% (v/v), up to 24 h after exposure. This observation is in agreement with the existing literature where 1% DMSO treatment for up to 40 h in U937 cells (the human myeloid leukemia cell line) did not show changes in Bax levels (46). Likewise, in an in vivo model, Dalton's lymphoma mice mRNA levels were assessed and the levels of Bax increased with the concomitant decrease of the Bcl‐2/ Bax ratio after DMSO treatment (7.5 g/kg ip; ref.…”

Section: Discussionsupporting

confidence: 93%

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Unexpected low‐dose toxicity of the universal solvent DMSO

et al. 2013

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Dimethyl sulfoxide (DMSO) is an important aprotic solvent that can solubilize a wide variety of otherwise poorly soluble polar and nonpolar molecules. This, coupled with its apparent low toxicity at concentrations <10%, has led to its ubiquitous use and widespread application. Here, we demonstrate that DMSO induces retinal apoptosis in vivo at low concentrations (5 μl intravitreally dosed DMSO in rat from a stock concentration of 1, 2, 4, and 8% v/v). Toxicity was confirmed in vitro in a retinal neuronal cell line, at DMSO concentrations >1% (v/v), using annexin V, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), and AlamarBlue cell viability assays. DMSO concentrations >10% (v/v) have recently been reported to cause cellular toxicity through plasma membrane pore formation. Here, we show the mechanism by which low concentrations (2-4% DMSO) induce caspase-3 independent neuronal death that involves apoptosis-inducing factor (AIF) translocation from mitochondria to the nucleus and poly-(ADP-ribose)-polymerase (PARP) activation. These results highlight safety concerns of using low concentrations of DMSO as a solvent for in vivo administration and in biological assays. We recommend that methods other than DMSO are employed for solubilizing drugs but, where no alternative exists, researchers compute absolute DMSO final concentrations and include an untreated control group in addition to DMSO vehicle control to check for solvent toxicity.

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Section: Discussionsupporting

confidence: 93%

“…16, 18), but most often, its absolute concentration is not reported (8, 9, 15–17). There is some functional, although no structural evidence that retinal toxicity is induced by low concentrations (0.6–8% v/v) of DMSO, but this study was based only on electrophysiology data (46).…”

Section: Discussionmentioning

confidence: 99%

Unexpected low‐dose toxicity of the universal solvent DMSO

et al. 2013

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“…Apigenin was administrated intraperitoneally dissolved in dimethyl sulfoxide solvent (DMSO). [2526] The exact consistency of the solution was: 5 mg apigenin + 0.2 ml DMSO + 0.3 ml NaCl 0.9%. Reperfusion was followed for 60, 120, and 240 minutes (AP60, AP120, and AP240 groups).…”

Section: Methodsmentioning

confidence: 99%

Intraperitoneal administration of apigenin in liver ischemia/reperfusion injury protective effects

Tsaroucha

Tsiaousidou

Ouzounidis

et al. 2016

Saudi J Gastroenterol

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Background/Aims:Hepatic injury caused by ischemia/reperfusion (I/R) is a clinical problem associated with major liver surgery. Among other flavonoids, apigenin has shown a promising effect on I/R cases. In this study, we have investigated the effects of apigenin after liver I/R injury in rats.Materials and Methods:Forty eight rats were randomized into the following eight groups: (1) Control-sham group: rats subjected to the surgical procedure, except for liver I/R; (2) DMSO group: rats subjected to surgery, except for liver I/R given the apigenin solvent dimethyl-sulfoxide intraperitoneally; (3) C60 group; (4) C120 group; (5) C240 group: rats underwent liver ischemia for 45 min followed by reperfusion for 60 min, 120 min, and 240 min; (6) AP60 group; (7) AP120 group; (8) AP240 group: rats underwent liver ischemia for 45 min, and then given apigenin (5 mg) intraperitoneally followed by reperfusion for 60 min, 120 min, and 240 min. Reverse transcription polymerase chain reaction was performed on liver tissues to measure BCL-2/BAX expression, enzyme-linked immunosorbent assay to measure M30/M65 and ICAM-1. Immunohistochemistry was used to identify M30 biomarker in liver tissues.Statistical Analysis:Quantitative variables were tested by Kolmogorov–Smirnov test, repeated measures analysis of variance/Friedman test. Gene levels were assessed by Student's t-test/Mann–Whitney U-test.Results:BCL-2 levels were significantly higher in I/R apigenin groups than in I/R control groups. BAX levels were lower in the AP240 group than in C240 group. Prolongation of reperfusion resulted in increased activation of M30. ICAM-1 levels were lower in the AP240 group than in C240 group.Conclusions:Apigenin seems to inhibit the process of apoptosis and ameliorate the hepatic I/R injury.

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“…APB and TPMPA were diluted using distilled H 2 O, whereas CNQX was mixed in the minimal volume of dimethyl sulphoxide (DMSO) that gave dilution. This DMSO concentration is known to have little effect on retinal function [25]. The concentrations stated represent the estimated final vitreal concentrations assuming complete dilution and a rat vitreal volume of 50 μ L [26].…”

Section: Methodsmentioning

confidence: 99%

Sustained and Transient Contributions to the Rat Dark-Adapted Electroretinogram b-Wave

Dang

Vingrys

2013

Journal of Ophthalmology

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The most dominant feature of the electroretinogram, the b-wave, is thought to reflect ON-bipolar cell responses. However, a number of studies suggest that the b-wave is made up of several components. We consider the composition of the rat b-wave by subtracting corneal negative components obtained using intravitreal application of pharmacological agents to remove postreceptoral responses. By analyzing the intensity-response characteristic of the PII across a range of fixed times during and after a light step, we find that the rat isolated PII has 2 components. The first has fast rise and decay characteristics with a low sensitivity to light. GABAc-mediated inhibitory pathways enhance this transient-ON component to manifest increased and deceased sensitivity to light at shorter (<160 ms) and longer times, respectively. The second component has slower temporal characteristics but is more sensitive to light. GABAc-mediated inhibition enhances this sustained-ON component but has little effect on its sensitivity to light. After stimulus offset, both transient and sustained components return to baseline, and a long latency sustained positive component becomes apparent. The light sensitivities of transient-ON and sustained-OFF components are consistent with activity arising from cone ON- and OFF-bipolar cells, whereas the sustained-ON component is likely to arise from rod bipolar cells.

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Dimethyl sulphoxide dose–response on rat retinal function

Cited by 22 publications

References 42 publications

Unexpected low‐dose toxicity of the universal solvent DMSO

Unexpected low‐dose toxicity of the universal solvent DMSO

Intraperitoneal administration of apigenin in liver ischemia/reperfusion injury protective effects

Sustained and Transient Contributions to the Rat Dark-Adapted Electroretinogram b-Wave

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