The hepatic handling of sulfobromphthalein in aging Fischer-344 rats: in vivo and in vitro studies

1985 ◽  
Vol 4 (1) ◽  
pp. 73-85 ◽  
Author(s):  
S. Kanai ◽  
K. Kitani ◽  
S. Fujita ◽  
H. Kitagawa
Keyword(s):  
In Vitro Studies ◽  
Fischer 344 Rats ◽  
Fischer 344

Central hypothyroidism is associated with advanced age in male Fischer 344/N rats: in vivo and in vitro studies.

Endocrinology ◽  
1992 ◽  
Vol 131 (6) ◽  
pp. 2672-2680 ◽  
Author(s):  
G Cizza ◽  
L S Brady ◽  
A E Calogero ◽  
G Bagdy ◽  
A B Lynn ◽  
...  
Keyword(s):  
In Vitro Studies ◽  
Advanced Age ◽  
Central Hypothyroidism ◽  
Fischer 344

scholarly journals Nephrotoxic Potential of Putative 3,5-Dichloroaniline (3,5-DCA) Metabolites and Biotransformation of 3,5-DCA in Isolated Kidney Cells from Fischer 344 Rats

2020 ◽  
Vol 22 (1) ◽  
pp. 292
Author(s):  
Gary O. Rankin ◽  
Christopher R. Racine ◽  
Monica A. Valentovic ◽  
Dianne K. Anestis
Keyword(s):  
Reactive Metabolites ◽  
Kidney Cells ◽  
Fischer 344 Rats ◽  
Isolated Kidney ◽  
Renal Metabolism ◽  
Fischer 344 ◽  
Primary Mechanism ◽  
Toxic Metabolites

The current study was designed to explore the in vitro nephrotoxic potential of four 3,5-dichloroaniline (3,5-DCA) metabolites (3,5-dichloroacetanilide, 3,5-DCAA; 3,5-dichlorophenylhydroxylamine, 3,5-DCPHA; 2-amino-4,6-dichlorophenol, 2-A-4,6-DCP; 3,5-dichloronitrobenzene, 3,5-DCNB) and to determine the renal metabolism of 3,5-DCA in vitro. In cytotoxicity testing, isolated kidney cells (IKC) from male Fischer 344 rats (~4 million/mL, 3 mL) were exposed to a metabolite (0–1.5 mM; up to 90 min) or vehicle. Of these metabolites, 3,5-DCPHA was the most potent nephrotoxicant, with 3,5-DCNB intermediate in nephrotoxic potential. 2-A-4,6-DCP and 3,5-DCAA were not cytotoxic. In separate experiments, 3,5-DCNB cytotoxicity was reduced by pretreating IKC with antioxidants and cytochrome P450, flavin monooxygenase and peroxidase inhibitors, while 3,5-DCPHA cytotoxicity was attenuated by two nucleophilic antioxidants (glutathione and N-acetyl-L-cysteine). Incubation of IKC with 3,5-DCA (0.5–1.0 mM, 90 min) produced only 3,5-DCAA and 3,5-DCNB as detectable metabolites. These data suggest that 3,5-DCNB and 3,5-DCPHA are potential nephrotoxic metabolites and may contribute to 3,5-DCA induced nephrotoxicity in vivo. In addition, the kidney can bioactivate 3,5-DCNB to toxic metabolites, and 3,5-DCPHA appears to generate reactive metabolites to contribute to 3,5-DCA nephrotoxicity. In vitro, N-oxidation of 3,5-DCA appears to be the primary mechanism of bioactivation of 3,5-DCA to nephrotoxic metabolites.

Cold- and norepinephrine-induced thermogenesis in younger and older Fischer 344 rats

1988 ◽  
Vol 254 (3) ◽  
pp. R457-R462 ◽  
Author(s):  
R. B. McDonald ◽  
B. A. Horwitz ◽  
J. S. Hamilton ◽  
J. S. Stern
Keyword(s):  
Body Mass ◽  
Mitochondrial Protein ◽  
Brown Fat ◽  
O2 Consumption ◽  
Fischer 344 Rats ◽  
Nonshivering Thermogenesis ◽  
Fischer 344 ◽  
Isolated Mitochondria

Older rats exposed to low environmental temperatures show attenuated thermogenesis. However, the mechanisms responsible for this attenuation are not clear. This investigation evaluated the possibility that reduced nonshivering thermogenic capacity is associated with this attenuation. O2 consumption was measured in male Fischer 344 rats ages 7 and 24 mo at thermoneutrality (26 degrees C), during exposure to cold (6 degrees C) for 2 h, and during norepinephrine (NE) infusion (an in vivo measure of nonshivering thermogenesis). In addition, the binding of GDP to isolated mitochondria of brown fat, an in vitro estimate of nonshivering thermogenesis, was also measured. Resting mass-independent O2 consumption (ml.min-1.g body mass -0.67) was not different between the two age groups. However, mass-independent O2 consumption was significantly greater in the younger vs. older rats during 2 h of cold exposure (younger, 2.86 +/- 0.19 l/kg body mass 0.67; older, 2.39 +/- 0.10 l/kg body mass 0.67) and during 20 min of maximum NE infusion (younger, 410.4 +/- 15.1 ml/kg body mass)] was greater in younger than ml/kg body mass 0.67). Brown fat mass [absolute (g) as well as relative (g tissue/kg body mass)] was greater in younger than in older rats. Furthermore, younger rats had significantly greater binding of GDP to isolated mitochondria of brown fat than did the older rats. This effect was true whether the data were expressed as nanomoles bound per milligram mitochondrial protein (32% lower in older rats), bound nanomoles recovered (57% lower), or bound picogram per kilogram body mass 0.67 (59% lower).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of L-arginine-derived nitric oxide synthesis on neuronal activity in nucleus tractus solitarius

1995 ◽  
Vol 268 (2) ◽  
pp. R487-R491 ◽  
Author(s):  
S. Ma ◽  
F. M. Abboud ◽  
R. B. Felder
Keyword(s):  
Nitric Oxide ◽  
Neuronal Activity ◽  
Nucleus Tractus Solitarius ◽  
Discharge Rate ◽  
Brain Slices ◽  
Spontaneous Discharge ◽  
Fischer 344 Rats ◽  
Fischer 344

The purpose of these studies was to determine the effects of L-arginine-derived nitric oxide (NO) synthesis on neuronal activity in solitary tract nucleus (NTS) neurons. Single unit activity was recorded extracellularly from medial NTS neurons in Fischer-344 rats in vivo and in vitro. In anesthetized rats with arterial pressure maintained constant, NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg iv), an inhibitor of NO synthesis, decreased the discharge rate in 12 of 14 neurons and increased the discharge rate in two. After injection of L-NAME, the slowing of neuronal activity began within 2-5 min, and maximal responses were observed 12-15 min after injection. The decreases in activity were reversed within 12-15 min with L-arginine (30 mg/kg iv) or immediately with nitroglycerin (NTG, 10-30 micrograms/kg iv). In superfused rat brain slices, the discharge rate was reduced by 1 mM L-NAME in seven neurons, increased in two, and unchanged in one. The decreases in discharge rate were reversed by 2 mM L-arginine (4 of 6 neurons) and by 10-30 microM NTG (6 of 7 neurons). The results show that L-arginine-derived NO can affect the spontaneous discharge rate of NTS neurons. We conclude that NO may influence the excitability of NTS neurons involved in central autonomic control.

The Venom of the Boomslang (Dispholidus Typus): In Vivo and in Vitro Studies

1969 ◽  
Vol 21 (02) ◽  
pp. 234-244 ◽  
Author(s):  
N Mackay ◽  
J.C Ferguson ◽  
Antonia Bagshawe ◽  
A.T.T Forrester ◽  
G.P Mcnicol
Keyword(s):  
In Vitro Studies

SummaryAn account is given of the effects of boomslang venom in man. Evidence was found of a fibrinolytic state apparently secondary to the coagulant action of the venom. These features rapidly responded to the administration of specific antivenom. In vitro studies, using a homogenate of boomslang parotids, confirmed the coagulant properties of the venom and showed them to be of much greater potency than the proteolytic actions.

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