Processing of leather using deep eutectic solvents

Processing of leather has an historical reputation as a chemically and energetically intensive process that produces large volumes of aqueous waste. Saline pollution combined with heavy-metal, dyes and acid and base streams make leather production an ecologically sensitive industry. The current study shows that a variety of deep eutectic solvents (DESs) may be used for the tanning, fatliquoring and dyeing of animal hides, being particularly useful for mineral (chromium) and vegetable tanning processes. The tanning agents are able to penetrate rapidly into the hide, driven by lyotropic swelling due to their high ionic strength. The samples are shown to have similar tanning agent content to the currently used aqueous chromium(III) sulfate solution; however, the waste metal content is shown to be significantly reduced. Incorporation of the DES Ethaline into the leather significantly alters the swelling properties of the leather increasing the flexibility and ductility of the material, therefore acting in the same manner as a fatliquor that lubricates or plasticizes the fibrous structure of the collagen. Ethaline was also used to transport a lysochromic dye throughout the cross section of the leather, and the hydrophobicity of the dye prevents leaching into the aqueous wash solution. Physical measurements show that leather processed using DESs have similar mechanical properties to that processed using conventional aqueous systems

Melatonin protects against heart ischemia-reperfusion injury by inhibiting mitochondrial permeability transition pore opening

Melatonin, a well-known antioxidant, has been shown to protect against ischemia-reperfusion myocardial damage. Mitochondrial permeability transition pore (MPTP) opening is an important event in cardiomyocyte cell death occurring during ischemia-reperfusion and therefore a possible target for cardioprotection. In the present study, we tested the hypothesis that melatonin could protect heart against ischemia-reperfusion injury by inhibiting MPTP opening. Isolated perfused rat hearts were subjected to global ischemia and reperfusion in the presence or absence of melatonin in a Langerdoff apparatus. Melatonin treatment significantly improves the functional recovery of Langerdoff hearts on reperfusion, reduces the infarct size, and decreases necrotic damage as shown by the reduced release of lactate dehydrogenase. Mitochondria isolated from melatonin-treated hearts are less sensitive than mitochondria from reperfused hearts to MPTP opening as demonstrated by their higher resistance to Ca(2+). Similar results were obtained following treatment of ischemic-reperfused rat heart with cyclosporine A, a known inhibitor of MPTP opening. In addition, melatonin prevents mitochondrial NAD(+) release and mitochondrial cytochrome c release and, as previously shown, cardiolipin oxidation associated with ischemia-reperfusion. Together, these results demonstrate that melatonin protects heart from reperfusion injury by inhibiting MPTP opening, probably via prevention of cardiolipin peroxidation