Effect of dimethyl sulfoxide (DMSO) on the electrocardiogram (ECG) in freely moving male Balb/c mice

Krämer, K.; Acker, S.A.B.E. van; Grimbergen, J.A.; Berg, Dirk–Jan van den; Vijgh, W.J.F. van der; Bast, Aalt

doi:10.1016/0306-3623(94)00300-c

Cited by 20 publications

(12 citation statements)

References 11 publications

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“…The peritoneum was exposed with a midline incision. A TA10EA-F20 implant (Datasciences, Minneapolis) was secured within the peritoneal cavity, and leads were implanted s.c. corresponding to position II (12,13). Mice were allowed to recover for 2 days after surgery.…”

Section: Methodsmentioning

confidence: 99%

Conditional lineage ablation to model human diseases

Lee

Morley

Huang

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

107

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Cell loss contributes to the pathogenesis of many inherited and acquired human diseases. We have developed a system to conditionally ablate cells of any lineage and developmental stage in the mouse by regulated expression of the diphtheria toxin A (DTA) gene by using tetracyclineresponsive promoters. As an example of this approach, we targeted expression of DTA to the hearts of adult mice to model structural abnormalities commonly observed in human cardiomyopathies. Induction of DTA expression resulted in cell loss, fibrosis, and chamber dilatation. As in many human cardiomyopathies, transgenic mice developed spontaneous arrhythmias in vivo, and programmed electrical stimulation of isolated-perfused transgenic hearts demonstrated a strikingly high incidence of spontaneous and inducible ventricular tachycardia. Affected mice showed marked perturbations of cardiac gap junction channel expression and localization, including a subset with disorganized epicardial activation patterns as revealed by optical action potential mapping. These studies provide important insights into mechanisms of arrhythmogenesis and suggest that conditional lineage ablation may have wide applicability for studies of disease pathogenesis.

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Section: Methodsmentioning

confidence: 99%

Conditional lineage ablation to model human diseases

Lee

Morley

Huang

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

107

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“…DMSO is a universal solvent for hydrophobic drugs and its cardio toxic affect is well established [30]. DMSO administration decreased the heart rate, S, ST and T interval and increased the RR and P amplitude in DMSO control group.…”

Section: Discussionmentioning

confidence: 98%

Repurposing Combination Therapy of Voacamine with Vincristine for Down Regulation of HIF-1α/FASN Co-Axis and PHD2 Activation in ER+ Mammary Neoplasia

Singh

Ansari

et al. 2020

Preprint

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Background: The current study was attempted to inquest the role of combination therapy of Voacamine and Vincristine for the prevention of mammary gland carcinoma through prolyl hydroxylase‐2 activation. The prolyl hydroxylase‐2 activation leads the downregulation of hypoxia‐inducible factor‐1α and fatty acid synthase. Over expression of hypoxia inducible factor-1α and fatty acid synthase is previously reported in solid tumor of mammary gland. Methods: After screening a battery of natural compounds which were similar to vincristine, vocamine was selected as a possible prolyl hydroxylase‐2 activator and justify its activity using 7, 12-Dimethylbenz[a]anthracene induced rat model. The combination therapy was evaluated for cardiac toxicity using hemodynamic profile. The angiogenic markers were evaluated using carmine staining. Monotherapy and combination therapy were also evaluated for liver and kidney toxicity through haematoxylin and eosin staining. The combination therapy also delineated the markers of oxidative stress favorably. Afterwards, the disruption of fatty acids was evaluated using gas chromatography. Results: The immunoblotting analysis validated that combination therapy has a potential to switch on the prolyl hydroxylase‐2 activity and thus initiate proteolytic degradation of hypoxia‐inducible factor‐1α and its consequence effects. The combination therapy also stimulated programmed cell death (apoptosis) in rapidly dividing cancer cells.Conclusion: The present study explores the role of voacamine in activation of prolyl hydroxylase‐2 which can decrease over expression of hypoxia‐inducible factor‐1α and fatty acid synthase in cells of mammary gland carcinoma.

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“…The relatively high proportion of DMSO was required to help dissolve the compound in a small volume of solvent. Although the concentration of DMSO is relatively high, similar solvent systems are used in animal studies where solubility of the test compounds is low . The activity of the dose ranged from 214 to 234 μCi.…”

Section: Methodsmentioning

confidence: 99%

Biodistribution (as determined by the radiolabelled equivalent) of a gold(III) bis(pyrrolide‐imine) Schiff base complex: a potential chemotherapeutic

Akerman

Munro

Mongane

et al. 2013

Labelled Comp Radiopharmac

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The biodistribution of an N2 N2 ' tetradentate gold(III) chelate, which is known to be cytotoxic towards a range of human cancer cell lines, was determined by a radiolabelled equivalent of the compound. The (198) Au-labelled gold(III) chelate of a bis(pyrrolide-imine) Schiff base ligand with a three-carbon di(azomethine) linkage was successfully synthesised with a high radiochemical yield of 73% and radiochemical purity of >95%. The high energy γ-ray emitted by the (198) Au nucleus was used to follow the biodistribution of the compound in vivo in six male Sprague Dawley rats on a gamma camera. The log Po/w value of the (nat) Au analogue, -1.92(2), showed that the compound is hydrophilic and therefore likely to largely remain in the blood pool. This was confirmed by the biodistribution study, which showed 21% of the injected dose (ID) remained in the blood pool 4.5 h after injection. This decreased to 10.8% over a 24-h period. The activity measured in the lungs, 1.48%ID/g, remained relatively constant over a 24-h period suggesting that the complex had accumulated in the lungs in the form of particulates, and could not be cleared by the test subjects. The t½ for the heart and lungs was greater than 24 h. Excretion of the test compound is seemingly via the kidneys, but is slow with approximately 30% of the ID excreted within 24 h.

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Effect of dimethyl sulfoxide (DMSO) on the electrocardiogram (ECG) in freely moving male Balb/c mice

Cited by 20 publications

References 11 publications

Conditional lineage ablation to model human diseases

Conditional lineage ablation to model human diseases

Repurposing Combination Therapy of Voacamine with Vincristine for Down Regulation of HIF-1α/FASN Co-Axis and PHD2 Activation in ER+ Mammary Neoplasia

Biodistribution (as determined by the radiolabelled equivalent) of a gold(III) bis(pyrrolide‐imine) Schiff base complex: a potential chemotherapeutic

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