Chloroquine pretreatment degradation

Discussion in 'Canadian Pharmacy' started by zadrot, 19-Mar-2020.

  1. zevgen User

    Chloroquine pretreatment degradation

    It has been shown to inhibit cell growth and/or to induce cell death in various types of cancer. 5-Fluorouracil (5-FU) is the chemotherapeutic agent of first choice in colorectal cancer, but in most cases, resistance to 5-FU develops through various mechanisms.

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    Chloroquine phosphate therapy 500 mg twice a day resulted in a decreased requirement for i.v. insulin 700 U/day as compared with the pretreatment requirement of 8400 U/ day. Accelerated insulin degradation in s.c. fat tissue of the patient before treatment with chloroquine was demonstrated. Chloroquine, a well-known antimalarial drug, posses pleitropic effects as well antiinflammatory, anticoagulant and vascular actions. The effects of chloroquine on renal function may involve significant increase in urine flow rate, glomerular filtration rate and sodium excretion, as well as stimulation of nitric oxide synthase. For example, chloroquine, a lysosomotropic agent, can prevent fusion of endosomes and lysosomes, and the resultant DNA degradation in the acidic environment in lysosomes through inhibition of acidification in late endosomes and lysosomes 11,15,62,63,65.

    HT-29 cells were treated with CQ and/or 5-FU, and their proliferative ability, apoptosis and autophagy induction effects, and the affection of the cell cycle were evaluated. Here, we focused on the combination of CQ as a mechanism to potentiate the inhibitory effect of 5-FU on human colon cancer cells.

    Chloroquine pretreatment degradation

    Autophagy a pathway that contributes to connexin degradation, Acute Pretreatment with Chloroquine Attenuates Renal I/R.

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  6. Chloroquine treatment of cells leads to accumulation of light chain 3-II LC3-II 1-3. This autophagy marker resides within autophagosomal membranes during the autophagic process and is degraded upon fusion with lysosomes. Chloroquine inhibition of these fusion events effectively blocks LC3-II degradation.

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    In addition, oxalate-induced p38 phosphorylation was significantly attenuated by chloroquine pretreatment but was markedly enhanced by rapamycin pretreatment, whereas the protective effect of chloroquine on rat renal tubular cell oxidative injury was partly reversed by a p38 protein kinase activator anisomycin. In conclusion it was found that the reactions taking place during pretreatment of biomass are complex and involve both degradation compounds and biomass structural elements. The present work has shed some light over the reactions and from this new insight a new type of pretreatment with anomeric protection was proposed and tested. To test if the degradation of albumin was taking place intracellularly in the lysosomal compartment of the tubular cell, we measured 125 I-albumin excretion in a separate group of rats after pretreatment of the ex vivo kidney preparation with chloroquine, a drug that inactivates lysosomal enzymes by increasing the lysosomal pH.

  7. Llevelin New Member

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