Superoxide dismutase, catalase and glutathione peroxidase activities in the lymphoid organs of diabetic rats

1994 ◽  
Vol 142 (1) ◽  
pp. 161-165 ◽  
Author(s):  
B Pereira ◽  
L F B Costa Rosa ◽  
D A Safi ◽  
E J H Bechara ◽  
R Curi
Keyword(s):  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Lymph Nodes ◽  
Diabetic Rats ◽  
Lymphoid Organs ◽  
Muscle Fibres ◽  
Antioxidant Enzyme Activities ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph ◽  
Gpx Activity

Abstract The effect of alloxan-induced diabetes on CuZn- and Mn-superoxide dismutase (SOD), catalase and glutathione peroxidase (GPX) activities, as well as the content of thiobarbituric acid reactive substances (TBARs) were examined in rat lymphoid organs (mesenteric lymph nodes (MLN), thymus and spleen) and, for comparison, red and white muscle fibres. The capacity for generation of reduced equivalents was also evaluated by measuring the activities of glucose-6-phosphate dehydrogenase (pentosephosphate pathway – cytosol) and citrate synthase (Krebs cycle – mitochondria). Diabetes raised the capacity for the generation of reducing equivalents in the lymphoid organs: in the mitochondria of the thymus and spleen and in the cytosol of the mesenteric lymph nodes and thymus. In muscles, diabetes reduced CuZn-SOD activity in soleus and raised the activity in gastrocnemius, and depressed the activities of catalase in soleus and of glutathione peroxidase in both soleus and gastrocnemius. In relation to the lymphoid organs, the spleen showed a decrease in the antioxidant enzyme activities (except for glutathione peroxidase), whereas the thymus showed an increased level (except for Mn-SOD), and the MLN presented a reduction in Mn-SOD and catalase activities and an increase in GPX activity caused by diabetes. The content of TBARs in the tissues followed the changes in GPX activity inversely: i.e. a decrease in the lymphoid organs (except in the spleen) and an increase in the muscles of diabetic rats compared with the control group. All these changes found in diabetic rats were reversed by insulin treatment and were not modified by the normalization of glycaemia. Journal of Endocrinology (1994) 142, 161–165

Control of superoxide dismutase, catalase and glutathione peroxidase activities in rat lymphoid organs by thyroid hormones

1994 ◽  
Vol 140 (1) ◽  
pp. 73-77 ◽  
Author(s):  
B Pereira ◽  
L F B P Costa Rosa ◽  
D A Safi ◽  
E J H Bechara ◽  
R Curi
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Thyroid Hormones ◽  
Citrate Synthase ◽  
Lipid Peroxide ◽  
Lymphoid Organs ◽  
Mesenteric Lymph Nodes ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Reducing Equivalents

Abstract This study examined the effect of experimental hyperand hypothyroidism on the superoxide dismutase, catalase and glutathione peroxidase activities of rat lymphoid organs (mesenteric lymph nodes, spleen and thymus) and muscles (soleus and gastrocnemius-white portion) for comparison. The capacity for the generation of reducing equivalents was also investigated: activities of glucose-6-phosphate dehydrogenase (pentose-phosphate pathway) and citrate synthase (Krebs cycle). Hyperthyroidism tended to enhance lipid peroxide content in all tissues. This effect may result from (1) a high capacity for the generation of reducing equivalents in cytosol and mitochondria and (2) a reduced activity of catalase in the lymphoid organs and of glutathione peroxidase in the muscles. The process of lipid peroxidation in these tissues caused by hyperthyroidism was probably slowed down by the augmentation of CuZn- and Mn-superoxide dismutase (Mn-SOD) activities observed under this condition. Hypothyroidism tended to diminish lipid peroxidation and did not affect citrate synthase and glucose-6-phosphate dehydrogenase activities in the lymphoid organs and muscles. Low levels of thyroid hormones tended to diminish Mn-SOD and glutathione peroxidase activities. These findings show that the thyroid hormones might be able to regulate the activities of CuZn- and Mn-SOD, and catalase and glutathione peroxidase in the lymphoid organs and skeletal muscles. Journal of Endocrinology (1994) 140, 73–77

scholarly journals Dynamics of Lymphocyte Populations duringTrypanosoma cruziInfection: From Thymocyte Depletion to Differential Cell Expansion/Contraction in Peripheral Lymphoid Organs

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Alexandre Morrot ◽  
Juliana Barreto de Albuquerque ◽  
Luiz Ricardo Berbert ◽  
Carla Eponina de Carvalho Pinto ◽  
Juliana de Meis ◽  
...  
Keyword(s):  
T Cell ◽  
Lymph Nodes ◽  
Chagas Disease ◽  
Negative Selection ◽  
Selection Process ◽  
Acute Infection ◽  
Lymphocyte Subpopulations ◽  
Lymphoid Organs ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph

The comprehension of the immune responses in infectious diseases is crucial for developing novel therapeutic strategies. Here, we review current findings on the dynamics of lymphocyte subpopulations following experimental acute infection byTrypanosoma cruzi, the causative agent of Chagas disease. In the thymus, although the negative selection process of the T-cell repertoire remains operational, there is a massive thymocyte depletion and abnormal release of immature CD4+CD8+cells to peripheral lymphoid organs, where they acquire an activated phenotype similar to activated effector or memory T cells. These cells apparently bypassed the negative selection process, and some of them are potentially autoimmune. In infected animals, an atrophy of mesenteric lymph nodes is also observed, in contrast with the lymphocyte expansion in spleen and subcutaneous lymph nodes, illustrating a complex and organ specific dynamics of lymphocyte subpopulations. Accordingly, T- and B-cell activation is seen in subcutaneous lymph nodes and spleen, but not in mesenteric lymph nodes. Lastly, although the function of peripheral CD4+CD8+T-cell population remains to be definedin vivo, their presence may contribute to the immunopathological events found in both murine and human Chagas disease.

scholarly journals Diabetes causes marked changes in lymphocyte metabolism

2002 ◽  
Vol 174 (1) ◽  
pp. 55-61 ◽  
Author(s):  
R Otton ◽  
R Curi ◽  
Keyword(s):  
Lymph Nodes ◽  
Palmitic Acid ◽  
Citrate Synthase ◽  
Diabetic Rats ◽  
Lymphocyte Function ◽  
Mesenteric Lymph Nodes ◽  
Diabetic State ◽  
Mesenteric Lymph ◽  
Glucose 6 Phosphate Dehydrogenase

An enhanced susceptibility to infections is well known to occur in a poorly controlled diabetic state. Since glucose and glutamine are essential for lymphocyte function, we investigated whether their metabolism is changed in lymphocytes obtained from mesenteric lymph nodes of alloxan-induced diabetic rats (40 mg/kg body weight). The activities of hexokinase, phosphofructokinase, glucose-6-phosphate dehydrogenase (G6PDH), citrate synthase and phosphate-dependent glutaminase were determined. Decarboxylation of metabolites [U-14C]-, [1-14C]- and [6-14C]-glucose, [1-14C]- and [2-14C]-pyruvic acid, [U-14C]-palmitic acid and [U-14C]-glutamine was evaluated in incubated lymphocytes isolated from mesenteric lymph nodes. The measurements were carried out in cells following three experimental protocols: (1) lymphocytes freshly obtained from control and alloxan-induced diabetic rats, (2) lymphocytes from insulin-treated (2 U/rat per day) diabetic rats and (3) lymphocytes obtained from control and diabetic rats and cultured in the presence of insulin (1 mU/ml) for 6 h. The activities of hexokinase, G6PDH and citrate synthase were decreased by the diabetic state, whereas that of phosphofructokinase was raised. Decarboxylation of [U-14C]- and [6-14C]-glucose, [1-14C]- and [2-14C]-pyruvate and [U-14C]-glutamine were also decreased in lymphocytes from diabetic rats, whereas [U-14C]-palmitic acid decarboxylation was increased. Insulin administration in vivo or added to the culture medium reversed the changes observed in freshly obtained lymphocytes. Alloxan-induced diabetes did change lymphocyte metabolism and this may be an important mechanism leading to impairment of lymphocyte function.

In situ demonstration of migration of dendritic cells released from rat small intestine to mesenteric lymph nodes

2001 ◽  
Vol 120 (5) ◽  
pp. A183-A183
Author(s):  
H KOBAYASHI ◽  
H NAGATA ◽  
S MIURA ◽  
T AZUMA ◽  
H SUZUKI ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Small Intestine ◽  
Lymph Nodes ◽  
Rat Small Intestine ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph

scholarly journals The microbiota is dispensable for the early stages of peripheral regulatory T cell induction within mesenteric lymph nodes

2021 ◽  
Author(s):  
Carolin Wiechers ◽  
Mangge Zou ◽  
Eric Galvez ◽  
Michael Beckstette ◽  
Maria Ebel ◽  
...  
Keyword(s):  
T Cell ◽  
Lymph Nodes ◽  
Regulatory T Cell ◽  
De Novo ◽  
Bacterial Species ◽  
Short Chain Fatty Acids ◽  
Mesenteric Lymph Nodes ◽  
Direct Role ◽  
Early Stages ◽  
Mesenteric Lymph

AbstractIntestinal Foxp3+ regulatory T cell (Treg) subsets are crucial players in tolerance to microbiota-derived and food-borne antigens, and compelling evidence suggests that the intestinal microbiota modulates their generation, functional specialization, and maintenance. Selected bacterial species and microbiota-derived metabolites, such as short-chain fatty acids (SCFAs), have been reported to promote Treg homeostasis in the intestinal lamina propria. Furthermore, gut-draining mesenteric lymph nodes (mLNs) are particularly efficient sites for the generation of peripherally induced Tregs (pTregs). Despite this knowledge, the direct role of the microbiota and their metabolites in the early stages of pTreg induction within mLNs is not fully elucidated. Here, using an adoptive transfer-based pTreg induction system, we demonstrate that neither transfer of a dysbiotic microbiota nor dietary SCFA supplementation modulated the pTreg induction capacity of mLNs. Even mice housed under germ-free (GF) conditions displayed equivalent pTreg induction within mLNs. Further molecular characterization of these de novo induced pTregs from mLNs by dissection of their transcriptomes and accessible chromatin regions revealed that the microbiota indeed has a limited impact and does not contribute to the initialization of the Treg-specific epigenetic landscape. Overall, our data suggest that the microbiota is dispensable for the early stages of pTreg induction within mLNs.

Pericolic mesenteric lymph nodes: an aid in distinguishing diverticulitis from cancer of the colon.

1997 ◽  
Vol 169 (5) ◽  
pp. 1253-1255 ◽  
Author(s):  
K N Chintapalli ◽  
C C Esola ◽  
S Chopra ◽  
A A Ghiatas ◽  
G D Dodd
Keyword(s):  
Lymph Nodes ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph
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