Suchergebnisse

AbstractMonosodium glutamate (MSG) is a widespread flavor enhancer and stabilizer in manufactured or packaged foods that possess myriad adverse effects. This study aimed to evaluate the effect of MSG on placental progesterone receptors and fetal development. Thirty pregnant Wistar Albino rats were divided into three groups (ten/each). The control group (G1) gavaged distilled water only, low-dose treated group (G2) gavaged 3 g/kg MSG, and high-dose treated group (G3) gavaged 6 g/kg MSG from 1st to 18th days of gestation, and all pregnant rats were sacrificed on the 19th day of gestation. The effect of MSG on fetal weights, crown vertebral length (CVL), placental weight, placental ghrelin expression, and fetal skeleton examination were estimated. MSG induced a significant decrease in fetal weights, CVL lengths, placental weight, and ghrelin expression in both treatment groups compared to the control group. Several parts of the fetal skeleton showed incomplete ossification and delayed chondrification in which high-dose maternally treated fetuses were more affected. Many degenerative changes were detected in both maternal and fetal liver and kidney tissues in MSG-treated groups. Moreover, MSG caused a significant increase in serum ALT, ALP, and creatinine levels in pregnant rats' blood. Serum progesterone was only elevated in G3 on the 19th day of gestation. This study showed that the administration of MSG during pregnancy adversely influences fetal growth and skeletal development and caused several biochemical and histological changes in the maternal and fetal liver and kidney tissues which assure the toxic and teratogenic effects of MSG.

Gcn5-related N-acetyltransferases catalyze the transfer of an acetyl group to a primary amino group of a wide class of substrates. Protonation of the amino group upon binding to the enzyme is necessary to activate the nucleophilic attack on the substrate. The process of glutamate binding to N-acetylglutamate synthase is considered using molecular modeling and quantum chemistry methods. It has been shown that deprotonation of the primary amino group of glutamate occurs upon binding to the active site of the enzyme with the participation of the side chain of the aspartate residue.

The objective of the study was to evaluate the effects of glutamine and glutamate (Gln/Glu) on the growth performance and immune response of nursery pigs fed different digestible lysine content. Two hundred and sixteen piglets, weaned at 21 days old, were assigned to a randomized block design according to their initial body weight (BW), in a 2 × 2 factorial arrangement with two levels of lysine (control-lys and low-lys) and two levels of Gln/Glu (0 and 12 g kg-1), with nine replicates. At 26 d, piglets consuming the low-lys diet not supplemented with Gln/Glu presented a higher (P < 0.01) incidence of diarrhea than the other treatments. From 21 to 32 d of age, the piglets fed the control-lys diets performed better than those fed low-lys diets (P < 0.01). From 21 to 42 d of age, there was a correlation (P < 0.01) between lysine level and Gln/Glu supplementation for average daily feed intake (ADFI) and feed conversion (FC). Gln/Glu supplementation improved (P < 0.05) the ADFI of pigs fed the low-lys diets, resulting in a higher (P < 0.01) average daily weight gain (ADG) and BW; however, worse (P < 0.05) FC. Piglets consuming control-lys diets had higher (P < 0.05) serum urea nitrogen concentration (SUN) and IgG than low-lys piglets. In addition, Gln/Glu supplementation correlated with higher (P < 0.01) SUN. Dietary supplementation of glutamine and glutamate improved the growth performance of weaned piglets from 21 to 42 days of age, regardless of the diets' lysine levels. In addition, reducing lysine levels 10% below the requirement negatively affects the growth performance and the immune response of nursery piglets.

The aim of work was to study the morphogenesis of pancreas in rats with glutamate-induced obesity and to evaluate the effects of melanin under these conditions. We included 45 newborn Wistarmale rats, divided into 3 groups of 15 animals each.1 group – newborns rats of intact group were administered with saline subcutaneously (s.c.) in the volume of 8 µl/g at 2–10th postnatal days. 2group – newborns rats of MSG-group received a solution of MSG (4,0 mg/g of body weight) s.c. at 2–10th postnatal days. 3 group – rats received aqueous solution of melanin in dose 1 mg/kg at volume 2,5 ml/kg per os (p.o.). Melanin was obtained from yeast-like fungi Nadsoniellanigra X1 strain from Ukrainian Antarctic station. Melanin administration was started at the age of 4 weeks just after wean and continued for 3 months intermittently alternating two- week course of introduction with two-week course of break. Within 4 months after birth, rats had a normal diet. Pancreas tissue was fixed in 10 % formalin, dehydrated and imbedded in paraffin wax. Paraffin sections of 5μm were cut and stained with hematoxylin and eosin. As low-grade inflammation is one of the leading mechanisms of pancreas lesion in obesity, the proinflammatory activation of pancreas cells was analyzed by immunohistochemical assessment of CD68 cells, NF-kB and TNF-α expression. The injection of glutamate sodium causes the development of obesity with an increase in the amount of visceral fat, an increase in the number of proinflammatory macrophages in it and an increase in the expression of NF-kB and TNFα. In the pancreas, there is a hyperplasia of the insular apparatus, associated with macrophage infiltration and an increase in the expression of COX-2. The introduction of melanin prevented the morphogenesis of the pancreas in animals from glutamate-induced obesity, leveling the activation of proinflammatory signaling paths.

Department of Chemistry, Government College, Burner, Barmer-344 001 Manuscript received 11 October 1982, revised 26 May 1986, accepted 18 June 1986 The mixed-ligand complexes of InIII with L-glutamate and L-methionine/L-valise/ L-proline have been investigated by polarographic technique. The cathodic reduction of mixed complexes involved three electrons, reversible and diffusion-controlled step. The logarthmic values of over all formation constants of In(L-glutamate)(L-methinni­nate), In(L-glutamate)(L-valinate) and In(L-glutamate)(L-prolinate) complexes were 16.78, 17.19 and 18 00, respectively. The positive values of logritham of mixing constant revealed that the mixed complexes were more stable than the parentbis­complexes.