Chitooligosaccharides (CHOS) are homo- or heterooligomers of N-acetylglucosamine and D-glucosamine. CHOS can be produced using chitin or chitosan as a starting material, using enzymatic conversions, chemical methods or combinations thereof. Production of well-defined CHOS-mixtures, or even pure CHOS, is of great interest since these oligosaccharides are thought to have several interesting bioactivities. Understanding the mechanisms underlying these bioactivities is of major importance. However, so far in-depth knowledge on the mode-of-action of CHOS is scarce, one major reason being that most published studies are done with badly characterized heterogeneous mixtures of CHOS. Production of CHOS that are well-defined in terms of length, degree of N-acetylation, and sequence is not straightforward. Here we provide an overview of techniques that may be used to produce and characterize reasonably well-defined CHOS fractions. We also present possible medical applications of CHOS, including tumor growth inhibition and inhibition of TH2-induced inflammation in asthma, as well as use as a bone-strengthener in osteoporosis, a vector for gene delivery, an antibacterial agent, an antifungal agent, an anti-malaria agent, or a hemostatic agent in wound-dressings. By using well-defined CHOS-mixtures it will become possible to obtain a better understanding of the mechanisms underlying these bioactivities.

/pdf/production-of-chitooligosaccharides-and-their-potential-4q4v2satlt.pdf

Production of Chitooligosaccharides and Their Potential Applications in Medicine

Physiological functions and pathogenic potential of uric acid: A review

Altered serum uric acid concentrations, both above and below normal levels, have been linked to a number of disease states. An abnormally high uric acid level has been correlated with gout, hypertension, cardiovascular disease, and renal disease, whereas a reduced uric acid concentration has been linked to multiple sclerosis, Parkinson's disease, Alzheimer's disease, and optic neuritis. Historically, uric acid has been considered a marker of these disease states. Recent studies, however, have provided evidence that uric acid may actually play a role in the development or progression of such diseases. As a result, the manipulation of uric acid concentrations is now either included in, or being investigated for, the treatment of a variety of disease states.

/pdf/altered-uric-acid-levels-and-disease-states-5ez13qg4sh.pdf

Altered Uric Acid Levels and Disease States

Oxidative stress contributes to dopaminergic neuron degeneration in Parkinson’s disease (PD).Urate, a potent antioxidant, could be neuroprotective. To determine whether higher plasma concentrations of urate predict a reduced risk of PD, we conducted a nested case-control study among participants in the Health Professional Follow-up Study, a cohort comprising over 18,000 men who provided blood samples in 1993–95. 84 incident cases of PD were diagnosed through 2000 and each was randomly matched to two controls by year of birth, race, and time of blood collection. Rate ratios (RR) of PD according to quartile of uricemia were estimated using conditional logistic regression. The mean urate concentration was 5.7mg/dL among cases and 6.1mg/dL among controls (p=0.01). After adjusting for age, smoking, and caffeine, the RR (95 percent confidence interval [CI]) of PD for the highest quartile of uricemia compared to the lowest was 0.43 (0.18, 1.02; p-for-trend=0.017). This association was stronger in analyses excluding cases diagnosed within 4 years (median) from blood collection (RR=0.17; 95 percent CI: 0.04, 0.69; p-for-trend=0.010). These results suggest that high plasma urate concentrations may decrease risk of PD and raise the possibility that interventions to increase plasma urate may reduce risk and delay the progression of PD.

Plasma Urate and Risk of Parkinson's Disease

Humans excrete uric acid as the final breakdown product of unwanted purine nucleotides. Urate scavenges potential harmful radicals in our body. However, in conjunction with genetic or environmental (especially dietary) factors, urate may cause gout, nephrolitiasis, hypertension, and vascular disease. Blood levels of urate are maintained by the balance between generation and excretion. Excretion requires specialized transporters located in renal proximal tubule cells, intestinal epithelial cells, and vascular smooth muscle cells. The recently identified human urate transporters URAT1, MRP4, OAT1, and OAT3 are thought to play central roles in homeostasis and may prove interesting targets for future drug development.

https://www.physiology.org/doi/pdf/10.1152/physiol.00039.2004

Molecular Physiology of Urate Transport

Several studies indicate that patients with multiple sclerosis (MS) have low serum levels of the endogenous antioxidant uric acid (UA), although it has not been established whether UA is primarily deficient or secondarily reduced due to its peroxynitrite scavenging activity. We measured serum urate levels in 124 MS patients and 124 age- and sex-matched controls with other neurological diseases. In addition, we compared UA levels when MS patients were stratified according to disease activity (by means of clinical examination and MRI), duration, disability and course. MS patients had significantly lower serum urate levels than controls (p= 0.001). However, UA levels did not significantly correlate with disease activity, duration, disability or course. Our study favors the view that reduced UA in MS is a primary, constitutive loss of protection against oxidative agents, which deserves further pathogenetic elucidation aimed at future therapeutic strategies.

Serum uric acid and multiple sclerosis.

Chitotriosidase and Alzheimer's disease.

MS-associated retrovirus in optic neuritis and non-inflammatory controls: a prevalence study in a Swedish population

Multiple sclerosis and chitotriosidase: a novel association

Constitutive Expression of human endogenous retroviruses in Normal and multiple sclerosis brains and glial cell cultures

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