Effects of iodotyrosines, thyronines, iodothyroacetic acids and thyromimetic analogues on in vitro copper-induced oxidation of low-density lipoproteins.

We studied the effect of different thyroid compounds [(I2, monoiodo-L-tyrosine (MIT), diiodo-L-tyrosine (DIT), L-thyronine (T0), 3,5-diiodo-L-thyronine (T2), 3,5,3'-triiodo-L-thyronine (T3), 3,3',5'-triiodo-L-thyronine (rT3), 3,5,3',5'-tetraiodo-L-thyronine (T4), 3,5-diiodothyroacetic acid (TA2), 3,5,3'-triiodothyroacetic acid (TA3) and 3,5,3',5'-tetraiodothyroacetic acid (TA4)] or thyromimetics [(3,5-dimethyl-3'-isopropyl-L-thyronine (DIMIT) and 3,5-diiodo-3'-isopropyl-thyroacetic acid (IpTA2)] on in vitro copper-induced oxidation of low-density lipoproteins (LDL). Human native LDL (0.05 g protein/L) oxidation was induced by 2.

Fatty acid oxidation and mechanical performance of volume-overloaded rat hearts.

Chronic volume overload was induced in 2-mo-old rats by surgical opening of the aortocaval fistula. Rats were killed 3 mo later and their hearts were atrially perfused. During the perfusions with 1.

[Prolonged fasting on the lipolytic activity of isolated adipocytes of the rat epididymis].

Male Wistar rats, 6-8 week old, were fasted for 72 hours. The in vitro lipolytic activity of epididymal adipocytes was measured in the presence of adrenalin (a alpha and beta adrenergic agonist), isoprenaline (a pure beta agonist), theophylline (a phosphodiesterase inhibitor) or UK 14304 (a alpha 2 adrenoceptor agonist) associated with adenosine deaminase. The basal lipolytic activity, expressed per 100 mg lipids, was higher in fasted adipocytes than in fed ones.

Influence of thyroid status on body weight gain, food intake and serum lipid levels in genetically obese Zucker rats.

Body weight gain, food intake and serum concentrations of total lipids, cholesterol, triglycerides, phospholipids and free fatty acids were measured in genetically obese and lean female Zucker rats after surgical thyroidectomy and treatment with 3,5,3'-triiodothyronine (T3) (3 micrograms/100 g body wt per day) for 4 wk. There were large differences in the major serum lipids between the control obese and lean rats. Obese rats were characterized by high levels of the various categories of lipids, especially of triglycerides.

[Effect of 3,3',5' triiodo-L-Thyronine (rT3) on the serum concentration of thyroid hormones in rats].

50, 100 or 150 micrograms/100 g body weight/day of very pure 3,3',5' triiodo-L-thyronine (rT3), obtained from a new synthetic method, was intraperitoneally administered in male Wistar rats for 5 weeks. Serum total thyroxine (T4), free thyroxine (FT4) and total 3,5,3' triiodo-L-thyronine (T3) concentrations were increased with all the doses of rT3. Free T3 (FT3) was also but non-significantly elevated.

Comparative effects of 3,5-dimethyl-3'-isopropyl-L-thyronine (DIMIT) and 3,5-diiodo-3'-isopropylthyroacetic acid (IpTA2) on body weight gain and lipid metabolism in genetically obese Zucker rats.

3,5-Dimethyl-3'-isopropyl-L-thyronine (DIMIT) and 3,5-diiodo-3'-isopropylthyroacetic acid (IpTA2), two thyroid hormone analogs, have been tested in genetically obese Zucker rats and their lean littermates, in comparison with thyroxine (T4) and triiodothyronine (T3) for their thyromimetic activities on body weight gain and lipid levels in serum and liver. The compounds were administered for 9 weeks by orogastric tube to 6- to 8-week-old animals. While body weight gain remained practically unchanged in the lean rats, it decreased significantly in the obese individuals, especially with IpTA2.

[Comparison of the lipolytic activity of adipocytes isolated from white adipose tissue in Zucker and Wistar rats. In vitro effects of 3,5,3'-triiodo-L-thyronine].

The in vitro effects of 3,5,3'-triiodo-L-thyronine (L-T3) on (-) epinephrine stimulated lipolytic activity were studied in adipocytes isolated from white adipose tissue of Zucker and Wistar male rats. Basic lipolytic activity was small and nearly insensitive to epinephrine in Zucker genetically obese rats. On the other hand, lipolytic activity was stimulated by epinephrine in Zucker lean rats and Wistar rats in the same way.

[Effects of lead poisoning on properties of brain mitochondria in young rats].

When the litters were 14 days old, wistar rat pups received lead ions. The suckling mother was fed by a powdered laboratory chow containing lead carbonate (1%, 2%, 4%). The intoxication was going on for 3 days to 9 weeks.

Dopamine and norepinephrine turnover in various regions of the rat brain after chronic manganese chloride administration.

Rats were treated with MnCl2 X 4H2O (1 mg/100 g/day, i.p.) for a period of 4 months.

[Effects of 3,5,3'-triiodothyroacetic acid (TRIAC) on protein metabolism of genetically obese or non-obese Zucker rats].

Genetically obese female rats (fa/fa) and their lean littermates (Fa/-) were given oral administration of 3,5,3-triiodothyroacetic acid (TRIAC) (20 micrograms/ 100 g of body weight/ day) during 4 weeks. Metabolism of proteins was evaluated in several organs and in skeletal muscle after intraperitoneal injection of 14C and 3H-leucine 6 days and 16 hrs respectively before the sacrifice of animals. We have determined radioactivity of 14C and 3H and the 3H/14C ratio.

[Kinetics of Mn2+ ion metabolism in rat hepatic tissue].

Intravenous injection of MnSO4 with 54Mn (0,33 mg/100 g) into rats showed that Mn2+ ions are transferred into intracellular organites and specially into mitochondria. The mitochondrial clearance curve of 54Mn has been analyzed. It is appeared that three compartments participate in the distribution of Mn2+.

[Effects of methylcyclopentadienyl manganese tricarbonyl (MMT) on rat liver mitochondria. II. Activity-structure relation (author's transl)].

The action of various manganese organic compounds, which are structural analogs of methylcyclopentadienyl manganese tricarbonyl (MMT), was investigated. Only the cyclopentadienyl manganese tricarbonyl compounds are effective inhibitors of mitochondrial respiration, but only when associated with NAD+-linked substrates. The manganese tricarbonyl group is required for this mitochondrial respiration inhibition.

[Effects of methylcyclopentadienyl manganese tricarbonyl (MMT) of rat liver mitochondria. I. Effects, in vitro, on the oxidative phosphorylation (author's transl)].

Methylcyclopentadienyl manganese tricarbonyl (MMT) is an effective inhibitor of mitochondrial respiration associated with NAD+-linked substrates. At concentrations which inhibit glutamate-malate oxidation (over 80% inhibition) succinate and tetramethylphenylenediamine (TMPD)-ascorbate are inhibited less than 25%. MMT inhibits both electron and energy transfer in mitochondria as revealed by the partial release of MMT inhibition by 2,4-dinitrophenol (DNP).