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Biomedical subjects

J Klimek

Publications and source records attributed to J Klimek.

At least 55 records · Page 3Linked to original sources
PubMed1985

The role of malic enzyme in the malate dependent biosynthesis of progesterone in the mitochondrial fraction of human term placenta.

Mitochondria isolated from human term placenta were able to form citrate from malate as the only added substrate. While mitochondria were incubated in the presence of Mn2+ the citrate formation was stimulated significantly both by NAD+ and NADP+ and was inhibited by hydroxymalonate, arsenite, butylmalonate and rotenone. It is concluded that NAD(P)-linked malic enzyme is involved in the conversion of malate to citrate in these mitochondria. It has also been shown that the conversion of cholesterol to progesterone by human term placental mitochondria incubated in the presence of malate was stimulated by NAD+ and NADP+ and inhibited by arsenite and fluorocitrate. This suggests that the stimulation by malate of progesterone biosynthesis depends not only on the generation of NADPH by NAD(P)-linked malic enzyme, but also on NADPH formed during further metabolism of pyruvate to isocitrate which is in turn efficiently oxidized by NADP+-linked isocitrate dehydrogenase.

Citrates↗
PubMed1985

Effect of a preventive program based on professional toothcleaning and fluoride application on caries and gingivitis.

The effect of a preventive program was studied in 12-14-yr-old children. 104 children (test group) participated in this program. After four visits in the first 6 wk, the children visited the oral hygienist five times a year to receive professional oral prophylactic treatment and instructions. Additionally a fluoride application (Duraphat) was given two times a year. Children of a control group (n = 117) received no prophylactic treatment. Diet was not controlled in either test or control group. After 2 yr mean caries increment amounted to 2.7 +/- 2.8 new DFS in the test group and 5.0 +/- 4.2 new DFS in the control group, respectively. The most pronounced differences between the two groups could be found on the proximal surfaces. In all, caries was reduced by 46% during the 2-yr period. Plaque accumulation and frequency of gingivitis were significantly reduced only in the test group (67% and 55%, resp.). The data revealed that the program reduced both caries and gingivitis to a remarkable extent.

Adolescent↗
PubMed1985

Fluoride uptake in plaque-covered enamel after treatment with the fluoride lacquer Duraphat.

The amount of alkali-soluble and alkali-insoluble fluoride was determined in human enamel after one- and six-hour treatments with Duraphat. The application was carried out on: (1) slightly demineralized enamel covered with artificial plaque, (2) cleaned, slightly demineralized enamel, and (3) sound enamel without pre-treatment. After a single Duraphat treatment lasting six hours, fluoride uptake was higher than after Duraphat treatment for just one hour in all experimental groups. More fluoride was acquired in both slightly demineralized, plaque-covered and slightly demineralized, cleaned enamel than in sound enamel. Plaque significantly hampered the formation of alkali-soluble fluoride precipitation on demineralized enamel, but its influence on the amount of fluoride taken up by the enamel was minor.

Calcium Fluoride↗
PubMed1983

Effect of paraquat on cytochrome P-450-dependent lipid peroxidation in bovine adrenal cortex mitochondria.

We have investigated the effect of paraquat (methyl viologen) on lipid peroxidation in bovine adrenal cortex mitochondria. Incubation of a buffered aerobic mixture of mitochondria in the presence of Fe2+ or NADPH resulted in the formation of lipid peroxides whose accumulation could be followed at 532 nm as malondialdehyde. Fe2+ stimulates lipid peroxidation in normal mitochondria and those in which enzymes have been inactivated with heat. In contrast, NADPH has a stimulatory effect only in normal mitochondria, but not in heat-treated mitochondria. These results indicate that NADPH-dependent lipid peroxidation is an enzymatic process. Paraquat strongly inhibits this enzymatic lipid peroxidation, but has no effect on the non-enzymatic Fe2+-dependent process. The chemiluminescence that accompanies the NADPH-dependent lipid peroxidation is also markedly decreased in the presence of paraquat. Superoxide dismutase, which removes superoxide anion efficiently, does not inhibit malondialdehyde production. The mechanism of the inhibition of the lipid peroxidation by paraquat has been examined. Paraquat has no effect on NADPH-2,6-dichlorophenolindophenol reductase and on NADPH-cytochrome c reductase activities in bovine adrenal cortex mitochondria. However, paraquat strongly inhibits the NADPH-dependent reduction of cytochrome P-450. These results suggest that the inhibitory effect of paraquat on NADPH-dependent lipid peroxidation in adrenal cortex mitochondria is due to a decrease in the level of reduced cytochrome P-450 probably by diverting electrons from cytochrome P-450. Cytochrome c, which can compete with P-450 for available electrons from adrenodoxin, like paraquat had an inhibitory effect on NADPH-dependent lipid peroxidation. Lipid peroxidation was also strongly inhibited by steroid hydroxylase inhibitors, e.g., amphenone B, aminoglutethimide and metyrapone.

Adrenal Cortex↗
PubMed1983

The relationship between NADPH-dependent lipid peroxidation and degradation of cytochrome P-450 in adrenal cortex mitochondria.

The relationship between NADPH-dependent lipid peroxidation and the degradation of cytochrome P-450 has been studied in bovine adrenal cortex mitochondria. Malondialdehyde formation is accompanied by a corresponding decrease in total cytochrome P-450 content. Inhibitors of lipid peroxidation also prevent the loss of cytochrome P-450, further demonstrating a direct relationship between NADPH-dependent lipid peroxidation and degradation of P-450. To differentiate between cytochrome P-450(11)beta and P-450scc, steroid-induced difference spectra were used to evaluate P-450 degradation. These measurements provide the first evidence that both P-450's are degraded during NADPH-dependent lipid peroxidation with P-450(11)beta being much more susceptible to this process.

Adrenal Cortex↗
PubMed1983

Progesterone biosynthesis supported by fatty acid oxidation in the mitochondrial fraction of human term placenta.

Oleic acid or oleoyl-CoA in the presence of bovine serum albumin, CoA, ATP, carnitine and malate were found to support progesterone biosynthesis from cholesterol in human term placental mitochondria. This fatty acid-dependent progesterone biosynthesis increased in the presence of adenine nucleotides and decreased after the addition of fluorocitrate. In the presence of rotenone only the stimulatory effect of ATP was maintained, whereas the inhibitory effect of fluorocitrate on the conversion of cholesterol to progesterone was abolished. Similar results were obtained when pyruvate was used as substrate instead of fatty acids. In the presence of antimycin, neither ATP nor fluorocitrate affected significantly the fatty acid-supported progesterone biosynthesis. These results indicate that oxidation of fatty acids stimulates progesterone biosynthesis by increasing the regeneration of the reducing equivalent necessary for the cholesterol side-chain cleavage reaction.

Acyl Coenzyme A↗