Products of sugar beet processing as raw materials for chemicals and biodegradable polymers.

This paper presents an overview of alternative uses for products of sugar beet processing, especially sucrose, as chemical raw materials for the production of biodegradable polymers. Traditionally, sucrose has not been considered as a chemical raw material, because of its use in the food industry and high sugar prices. Beet pulp and beetroot leaves have also not been considered as raw materials for chemical production processes until recently. However, current changes in the European sugar market could lead to falling demand and overproduction of sucrose. Increases in the production of white sugar will also increase the production of waste biomass, as a result of the processing of larger quantities of sugar beet. This creates an opportunity for the development of new chemical technologies based on the use of products of sugar beet processing as raw materials. Promising methods for producing functionalized materials include the acidic hydrolysis of sugars (sucrose, biomass polysaccharides), the catalytic dehydration of monosaccharides to HMF followed by catalytic oxidation of HMF to FDCA and polymerization to biodegradable polymers. The technologies reviewed in this article will be of interest both to industry and science.

Dopamine-induced stress signaling in COS-7 cells transfected with selectively vulnerable muscarinic receptor subtypes is partially mediated via the i3 loop and antagonized by blueberry extract.

Muscarinic receptors (MAChRs) are intimately involved in various aspects of both neuronal and vascular functioning, and there is selective oxidative stress sensitivity (OSS) among MAChR subtypes, with M1, M2, and M4 showing>OSS. OSS was assessed by determining the loss of ability of the cell to extrude or sequester Ca2+ following oxotremorine-induced depolarization following exposure to dopamine (DA) subtypes in transfected COS-7 cells. This OSS can be prevented by pretreatment with blueberry (BB) extract. Present studies were carried out to determine BB treatment of the cells transfected with wild type, truncated or chimeric [where the i3 loop of one receptor was switched with the i3 loop of the other; i.e., M1(M3i3) and M3(M1i3)] receptors would alter DA-induced changes in calcium buffering and would confer protection through alterations in pMAPK, pCREB or PKC signaling. These findings also suggest that BB may antagonize OS effects by lowering activation of pCREB and possibly PKCgamma induced by DA. In the truncated and chimeric receptors, results indicated that BB reduced OSS in response to DA in M1-transfected cells. However, BBs were also effective in preventing these Ca2+ buffering deficits in cells transfected with M1 receptors in which the i3 loop had been removed, but only partially enhanced the protective effects of the M3 i3 loop in the M1(M3i3) chimerics. A similar partial effect of BBs was seen in the M3(M1i3) chimerics which showed increased OSS in response to DA. It appears that antioxidants found in BBs might be targeting additional sites on these chimerics to decrease OSS.

Blueberry extract alters oxidative stress-mediated signaling in COS-7 cells transfected with selectively vulnerable muscarinic receptor subtypes.

Previous research has indicated that selective vulnerability to oxidative stress may be important in determining regional differences in functional declines in neuronal aging. Oxidative stress vulnerability may involve selective deficits in Ca2+ buffering (Ca2+ recovery time following oxotremorine application) to oxidative stress, determined in-part by receptor subtype with M1, M2 and M4 AChR showing greater oxidative stress-induced loss [via dopamine (DA) exposure for 4 hrs] of Ca2+ recovery time than that seen in M3 or M5 cells. Deficits were antagonized by pre-treating M1, M2, or M4 AChR-transfected cells with blueberry (BB) extract. Thus, we assessed whether these differences in oxidative stress vulnerability might involve differential patterns of DA-induced protein kinase (PKCalpha, PKCgamma) and/or cyclic AMP response element binding protein (CREB) activation, and whether these differences might be altered by BB treatment. M1 or M3 AChR-transfected COS-7 cells were exposed to 1 mM DA, and activation of phospho-(p) mitogen-activated protein kinase (MAPK) signaling was examined by immunoblotting analyses. The results showed that DA increased pCREB and pPKCgamma for both M1- and M3-transfected cells, and BBs decreased these DA-induced alterations, when measured by immunoblotting techniques. Taken together these findings suggest that M1/M3 oxidative stress sensitivity differences may involve differential signaling in pMAPK and pCREB under oxidative stress conditions, suggesting that the native protection in these receptors against oxidative stress and inflammation may be derived from reduced activation. These findings also suggest that BB may antagonize oxidative stress effects induced by DA in M1-transfected cells by lowering activation of pCREB, and possibly pPKCgamma.

Oxidative stress protection and vulnerability in aging: putative nutritional implications for intervention.

Research indicates that vulnerability to oxidative stress (OSV) may increase in aging, suggesting that age-related neurodegenerative diseases such as Alzheimer's disease (AD) or vascular dementia (VAD) may be superimposed upon a vulnerable neuronal environment. Determinations in cell models have suggested that the enhanced OSV may be the result of, (a) increases in membrane lipids, especially sphingomyelin and the sphingomyelin metabolite, sphingosine-1-phosphate, (b) decreases in glutathione, and (c) CNS distribution of OS-sensitive neuronal muscarinic receptor subtypes (e.g. M1, M2 and M4). These changes appear to enhance, (a) decrements in cellular calcium buffering following KCl-induced depolarization, and (b) cell death under OS conditions. Among the most effective agents that antagonized cellular OSV were the combination of polyphenolics found in fruits (e.g. blueberry extract) with high antioxidant activity. Subsequent experiments using dietary supplementation with fruit (strawberry) or vegetable (spinach) extracts have shown that such extracts are also effective in forestalling and reversing the deleterious effects of behavioral aging in F344 rats. Thus, it appears that the beneficial effects of the polyphenolics found in fruits and vegetables in neuronal aging and behavior may be similar to those seen with respect to carcinogenesis and cardiovascular disease.

Reversals of age-related declines in neuronal signal transduction, cognitive, and motor behavioral deficits with blueberry, spinach, or strawberry dietary supplementation.

Ample research indicates that age-related neuronal-behavioral decrements are the result of oxidative stress that may be ameliorated by antioxidants. Our previous study had shown that rats given dietary supplements of fruit and vegetable extracts with high antioxidant activity for 8 months beginning at 6 months of age retarded age-related declines in neuronal and cognitive function. The present study showed that such supplements (strawberry, spinach, or blueberry at 14.8, 9.1, or 18.6 gm of dried aqueous extract per kilogram of diet, respectively) fed for 8 weeks to 19-month-old Fischer 344 rats were also effective in reversing age-related deficits in several neuronal and behavioral parameters including: oxotremorine enhancement of K(+)-evoked release of dopamine from striatal slices, carbachol-stimulated GTPase activity, striatal Ca(45) buffering in striatal synaptosomes, motor behavioral performance on the rod walking and accelerod tasks, and Morris water maze performance. These findings suggest that, in addition to their known beneficial effects on cancer and heart disease, phytochemicals present in antioxidant-rich foods may be beneficial in reversing the course of neuronal and behavioral aging.

Ral and Rab3a are major GTP-binding proteins of axonal rapid transport and synaptic vesicles and do not redistribute following depolarization stimulated synaptosomal exocytosis.

We have employed high-resolution SDS polyacrylamide gels to demonstrate that there are two major low-molecular-weight GTP-binding proteins associated with axonal membranes including synaptic vesicles, rapid transported membranes and clathrin-coated vesicles. We demonstrate that one of the major proteins is Ral and that the other is Rab3A. Following the depolarization of synaptosomes resulting in increased neurotransmitter release, we see no significant dissociation of either Ral or Rab3a from synaptic vesicle derived membranes in contrast to results reported previously.

Low molecular weight GTP-binding proteins are associated with neuronal organelles involved in rapid axonal transport and exocytosis.

Recent evidence suggests that low molecular weight GTP-binding proteins may play important roles in a variety of membrane transport processes. In order to address the question of whether these proteins are involved in transport processes in the nerve axon, we have assessed their presence in rapid transport membranes from rabbit optic nerve. We report the characterization of a group of low molecular weight GTP-binding proteins which are constituents of rapid transport vesicles. Although these proteins are components of rapid transport vesicles, they are apparently not major rapidly transported species. They are localized in cytosolic as well as in membrane fractions of axons, and the membrane-associated form behaves as an integral membrane protein(s). These proteins are also found in association with a variety of vesicular and organellar components of neurons including coated vesicles, synaptic vesicles, synaptic plasma membranes, and mitochondria. We discuss the possible roles of these proteins in rapid axonal transport and exocytosis.

Differential coupling of smooth muscle and liver vasopressin (V1) receptors to guanine nucleotide binding proteins.

We report the reconstitution of the smooth muscle vasopressin V1 receptor functionally coupled to a pertussis toxin-insensitive guanine nucleotide-binding protein. This V1 receptor was spontaneously coupled to this guanine nucleotide-binding protein upon solubilization in the absence of agonist, in contrast to our earlier report on the liver V1 receptor, which required agonist for coupling. The smooth muscle V1 receptor was reconstituted as a high affinity receptor (Kd = 5 nM), with a slow rate of agonist dissociation. Upon the addition of guanosine 5'-thiotriphosphate, there was a decrease in receptor affinity (Kd = 30 nM) concomitant with an increase in the rate of ligand dissociation. The ability of the smooth muscle V1 receptor to spontaneously couple to a guanine nucleotide-binding protein(s) suggests that in the absence of agonist it exists as a high affinity receptor. The smooth muscle V1 receptor may, therefore, be more sensitive to plasma concentrations of vasopressin than its liver homologue.