A new colorimetric technique for the estimation of Vitamin C using Folin Phenol Reagent

Department of Biochemistry, Panjab University, Chandigarh-160 014, India
Analytical Biochemistry (Impact Factor: 2.22). 12/1982; 127(1):178-82. DOI: 10.1016/0003-2697(82)90162-2
Source: PubMed

ABSTRACT A new colorimetric technique for the estimation of ascorbic acid by using Folin phenol reagent has been developed. The absorption maximum of the color developed by the interaction of ascorbic acid with Folin reagent is 760 nm. The technique obeys the Beer-Lambert law up to a concentration of 45 μg ascorbic acid as shown by the standard curve. The color developed has been found to be stable up to 18 h. Recovery experiments showed that the technique is almost 100% efficient. The development of the color is not obstructed by glucose, glutathione, bovine serum albumin, urea, cysteine, adenine, guanine, cytosine, uracil, sulfosalicylic acid, thymol, or oxyhemoglobin, which are compounds suspected of interfering in routine analysis. The technique is simple, quick, and efficient and can be employed for the estimation of ascorbic acid in a wide variety of biological materials.

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    • "(ii) pH: the pH of pickle solution and pickled roselle calyces were determined using digital pH meter. (iii) Anthocyanin content: the amount of anthocyanin in the fresh and pickled roselle calyces were determined at 520 nm using spectrophotometer based on delphinidin-3-glucoside. (iv) Ascorbic acid: the amount of ascorbic acid were determined according to Jagota and Dani (1982) "
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    • "In our study, NO produced following focal ischemia/reperfusion injury was quantified by measuring nitrite which is been a stable end product of NO (Jagota and Dani, 1982). A rise in the nitrite level is being evident in the region of ischemic insult of brain after 10 min following cerebral ischemia and declined to basal levels after 60 min (Stirling et al., 2005). "
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    ABSTRACT: Aim Aquaporin-4(AQP4) expression in brain with relation to edema formation following focal cerebral ischemia was investigated. Studies have shown that brain edema is one of the significant factors in worsening stroke outcomes. While many mechanisms may aggravate brain injury, one such potential system may involve AQP4 up regulation in stroke patients that could result in increased edema formation. Post administration of melatonin following ischemic stroke reduces AQP4 mediated brain edema and confer neuroprotection. Materials and Methods An in-silico approach was undertaken to confirm effective melatonin-AQP4 binding. Rats were treated with 5mg/kg, i.p. melatonin OR placebo at 30 min prior, 60 min post and 120 min post 60 minutes of MCAO followed by 24 hour reperfusion. Rats were evaluated for battery of neurological and motor function tests just before sacrifice. Brains were harvested for infarct size estimation, water content measurement, biochemical analysis, apoptosis study and western blot experiments. Key findings Melatonin at sixty minutes post ischemia rendered neuroprotection as evident by reduction in cerebral infarct volume, improvement in motor and neurological deficit and reduction in brain edema. Furthermore, ischemia induced surge in levels of nitrite and MDA were also found to be significantly reduced in ischemic brain regions in treated animals. Melatonin potentiated intrinsic antioxidant status, inhibited acid mediated rise in intracellular calcium levels, decreased apoptotic cell death and also markedly inhibited protein kinase C influenced AQP4 expression in the cerebral cortex and dorsal striatum. Significance Melatonin confer neuroprotection by Protein Kinase C mediated AQP4 inhibition in ischemic stroke.
    Life sciences 04/2014; 100(2). DOI:10.1016/j.lfs.2014.01.085 · 2.30 Impact Factor
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    • "The proteins and insoluble material were clarified by centrifugation. The supernatant was dried and ascorbic acid estimated with a colorimetric assay as described (Jagota and Dani, 1982). Cellular levels of total and oxidized glutathione were measured fluorometrically using the DTNB glutathione reductase recycling assay as described previously (Griffith, 1980). "
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    ABSTRACT: Endoplasmic reticulum (ER) thiol oxidases initiate a disulfide relay to oxidatively fold secreted proteins. We found that combined loss-of-function mutations in genes encoding the ER thiol oxidases ERO1α, ERO1β, and PRDX4 compromised the extracellular matrix in mice and interfered with the intracellular maturation of procollagen. These severe abnormalities were associated with an unexpectedly modest delay in disulfide bond formation in secreted proteins but a profound, 5-fold lower procollagen 4-hydroxyproline content and enhanced cysteinyl sulfenic acid modification of ER proteins. Tissue ascorbic acid content was lower in mutant mice, and ascorbic acid supplementation improved procollagen maturation and lowered sulfenic acid content in vivo. In vitro, the presence of a sulfenic acid donor accelerated the oxidative inactivation of ascorbate by an H(2)O(2)-generating system. Compromised ER disulfide relay thus exposes protein thiols to competing oxidation to sulfenic acid, resulting in depletion of ascorbic acid, impaired procollagen proline 4-hydroxylation, and a noncanonical form of scurvy.
    Molecular cell 09/2012; 48(1):39-51. DOI:10.1016/j.molcel.2012.08.010 · 14.46 Impact Factor
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