Role of Nitric Oxide in Down-Regulation of CYP2B1 Protein, but Not RNA, in Primary Cultures of Rat Hepatocytes

2001 ◽  
Vol 60 (1) ◽  
pp. 209-216 ◽  
Author(s):  
Luc Ferrari ◽  
Ning Peng ◽  
James R. Halpert ◽  
Edward T. Morgan
Keyword(s):  
Nitric Oxide ◽  
Primary Cultures ◽  
Rat Hepatocytes ◽  
Down Regulation

scholarly journals Overexpression of CuZn superoxide dismutase protects RAW 264.7 macrophages against nitric oxide cytotoxicity

1999 ◽  
Vol 338 (2) ◽  
pp. 295-303 ◽  
Author(s):  
Florian BROCKHAUS ◽  
Bernhard BRÜNE
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Superoxide Dismutase ◽  
Uric Acid ◽  
No Synthase ◽  
Raw 264.7 ◽  
Down Regulation ◽  
Raw 264.7 Macrophages ◽  
Inducible No Synthase

Initiation of nitric oxide (NO•)-mediated apoptotic cell death in RAW 264.7 macrophages is associated with up-regulation of mitochondrial manganese superoxide dismutase (MnSOD; SOD2) and down-regulation of cytosolic copper zinc superoxide dismutase (CuZnSOD; SOD1) at their individual mRNA and protein levels. To evaluate the decreased CuZnSOD expression and the initiation of apoptosis we stably transfected macrophages to overexpress human CuZnSOD. Individual clones revealed a 2-fold increase in CuZnSOD activity. Expression of a functional and thus protective CuZnSOD was verified by attenuated superoxide (O2•-)-mediated apoptotic as well as necrotic cell death. In this study we showed that SOD-overexpressing macrophages (R-SOD1-12) were also protected against NO•-initiated programmed cell death. Protection was substantial towards NO• derived from exogenously added NO donors or when NO• was generated by inducible NO synthase activation, and was evident at the level of p53 accumulation, caspase activation and DNA fragmentation. Stimulation of parent and SOD-overexpressing cells with a combination of lipopolysaccharide and murine interferon γ produced equivalent amounts of nitrite/nitrate, which ruled out attenuated inducible NO• synthase activity during protection. Because protection by a O2•--scavenging system during NO•-intoxication implies a role of NO• and O2•- in the progression of cell damage, we used uric acid to delineate the role of peroxynitrite during NO•-elicited apoptosis. The peroxynitrite scavenger uric acid left S-nitrosoglutathione or spermine-NO-elicited apoptosis unaltered, blocking only 3-morpholinosydnonimine-mediated cell death. As a result we exclude peroxynitrite from contributing, to any major extent, to NO•-mediated apoptosis. Therefore protection observed with CuZnSOD overexpression is unlikely to stem from interference with peroxynitrite formation and/or action. Unequivocally, the down-regulation of CuZnSOD is associated with NO• cytotoxicity, whereas CuZnSOD overexpression protects macrophages from apoptosis.

Enalapril cytotoxicity in primary cultures of rat hepatocytes. II. Role of glutathione

1991 ◽  
Vol 58 (3) ◽  
pp. 269-277 ◽  
Author(s):  
Malle Jurima-Romet ◽  
Hide S. Huang ◽  
Charles J. Paul ◽  
Barry H. Thomas
Keyword(s):  
Primary Cultures ◽  
Rat Hepatocytes

scholarly journals Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism.

1994 ◽  
Vol 180 (1) ◽  
pp. 365-369 ◽  
Author(s):  
S C Lee ◽  
D W Dickson ◽  
C F Brosnan ◽  
A Casadevall
Keyword(s):  
Nitric Oxide ◽  
Cryptococcus Neoformans ◽  
Interleukin 1 ◽  
Primary Cultures ◽  
Immune Deficiency Syndrome ◽  
Deficiency Syndrome ◽  
Effector Cells ◽  
Human Astrocytes ◽  
Life Threatening

Cryptococcus neoformans is an opportunistic fungus that causes life-threatening meningoencephalitis in 5-10% of patients with acquired immune deficiency syndrome. Cryptococcal meningoencephalitis is characterized by a lymphohistiocytic infiltrate, accumulation of encapsulated forms of C. neoformans, and varying degrees of glial reaction. Little is known about the contribution of endogenous central nervous system cells to the pathogenesis of cryptococcal infections. In this study, we investigated the role of astrocytes as potential effector cells against C. neoformans. Primary cultures of human fetal astrocytes, activated with interleukin 1 beta plus interferon gamma inhibited the growth of C. neoformans. The inhibition of C. neoformans growth was paralleled by production of nitrite, and reversed by the inhibitors of nitric oxide (NO.) synthase, NG-methyl-mono-arginine and NG-nitro-arginine methyl ester. The results suggest a novel function for human astrocytes in host defence and provide a precedent for the use of NO. as an antimicrobial effector molecule by human cells.

Down-Regulation of Insulin Binding by Human and Rat Hepatocytes in Primary Culture: The Possible Role of Insulin Internalization and Degradation*

Endocrinology ◽  
1984 ◽  
Vol 114 (1) ◽  
pp. 37-43 ◽  
Author(s):  
N. KALANT ◽  
S. OZAKI ◽  
H. MAEKUBO ◽  
B. MITMAKER ◽  
M. COHEN-KHALLAS
Keyword(s):  
Primary Culture ◽  
Rat Hepatocytes ◽  
Insulin Binding ◽  
Down Regulation

Role of endogenous nitric oxide in liver-specific functions and survival of cultured rat hepatocytes

Xenobiotica ◽  
2001 ◽  
Vol 31 (5) ◽  
pp. 249-264 ◽  
Author(s):  
M. T. Donato ◽  
X. Ponsoda ◽  
E. O’Connor ◽  
J. V. Castell ◽  
M. J. Gómez-Lechón
Keyword(s):  
Nitric Oxide ◽  
Rat Hepatocytes ◽  
Endogenous Nitric Oxide ◽  
Cultured Rat Hepatocytes

Leptin modulates nitric oxide production and lipid metabolism in human placenta

2006 ◽  
Vol 18 (4) ◽  
pp. 425 ◽  
Author(s):  
Verónica White ◽  
Elida González ◽  
Evangelina Capobianco ◽  
Carolina Pustovrh ◽  
Nora Martínez ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lipid Metabolism ◽  
Human Placenta ◽  
De Novo ◽  
Primary Cultures ◽  
Lipid Synthesis ◽  
No Production ◽  
Dependent Manner ◽  
Lipid Catabolism

Leptin has significant effects on appetite, energy expenditure, lipid mobilisation and reproduction. During pregnancy, leptin is produced in the placenta, a tissue in which leptin receptors are highly expressed, suggesting autocrine/paracrine functions for this hormone. In the present study, a putative role of leptin as a regulator of nitric oxide (NO) production and lipid metabolism was evaluated in term human placenta. We demonstrated that leptin enhanced NO production in human placental explants (P < 0.01). Although leptin did not modify the placental levels of cholesteryl esters and phospholipids, leptin decreased levels of triglycerides (P < 0.01) and cholesterol (P < 0.001) in term human placenta. The effect of leptin on lipid mass seems to be independent of the modulation of de novo lipid synthesis because leptin did not modify the incorporation of 14C-acetate into any of the lipids evaluated. We investigated the effects of leptin on placental lipid catabolism and found that in both term human placental explants and primary cultures of trophoblastic cells, leptin increased glycerol release, an index of the hydrolysis of esterified lipids, in a dose-dependent manner. In conclusion, we have shown that leptin affects NO production and lipid catabolism in human placenta, providing supportive evidence for a role of leptin in placental functions that would determine the transfer of nutrients to the developing fetus.

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