Drugs online research references
Exp Mol Pathol. 1989 Jun;50(3):385-97.
Ultrastructural alterations in ovaries from nifurtimox or benznidazole-treated rats: their relation to ovarian nitroreductive biotransformation of both drugs.
de Castro CR, de Toranzo EG, Bernacchi AS, Carbone M, Castro JA.
Centro de Investigaciones Toxicologicas (CEITOX), CITEFA/CONICET, Buenos Aires, Argentina.
Chagas' disease is a parasitic chronic condition affecting several million people in Latin America. Two drugs are used in the chemotherapy of Chagas' disease: nifurtimox (Nfx) and benznidazole (Bz). Both are nitroderivatives whose deleterious effects are related to their reductive biotransformation. In this work we report that rat ovaries exhibited Bz and Nfx nitroreductase activity. The Bz nitroreductase was only found in the mitochondrial fraction and was partially inhibited by CO. The Nfx nitroreductase activity was maximal in ovarian mitochondria but was also present in microsomes and in the cytosol. The microsomal enzyme was completely inhibited by CO while that in mitochondria was only partially inhibited by CO. The cytosolic activity only proceeded using hypoxanthine as substrate and was inhibited by allopurinol. The cytosolic activity was able to proceed in part under oxygen. All the other Bz or Nfx nitroreductases were completely inhibited by atmospheric oxygen. The potential participation of cytochrome P450, flavoenzymes, iron-sulfur-protein, and xanthinooxidase in both nitroreductive processes is discussed. The administration of either Nfx or Bz to female rats produced ultrastructural degenerative effects in the different cell types of ovaries. Specific alterations such as swelling, disruption, disorganization, and loss of matrix components were observed in ovarian mitochondria. These alterations occurred irrespectively of the ovarian cycle stage. The potential reproductive toxicological consequences of Bz or Nfx administration are analyzed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2721655&dopt=Abstract
Metabolism. 1989 May;38(5):410-8.
Adenine nucleotide turnover in hypoxanthine-guanine phosphoribosyl-transferase deficiency: evidence for an increased contribution of purine biosynthesis de novo.
Puig JG, Jimenez ML, Mateos FA, Fox IH.
Department of Internal Medicine, La Paz University Hospital, Universidad Autonoma, Madrid, Spain.
This study examined whether increased purine biosynthesis de novo in HGPRT deficiency contributes to adenine nucleotide formation compared with normal subjects. Four HGPRT deficient patients and four normal subjects received intravenously 10 to 25 microCi of [8-14C]adenine to radiolabel the adenine nucleotide pool followed five days later by a rapid infusion of fructose to stimulate purine nucleotide degradation. Fructose infusion increased urinary radioactivity in the enzyme-deficient patients to 141% +/- 13% (mean +/- SEM) of the baseline values compared with 1,067% +/- 102% in normal subjects (P less than .01). The absolute mean increase in total urinary purines in the patients was 17.96 +/- 3.36 and 10.38 +/- 3.80 mmol/g creatinine in controls (P less than .05). The apparent specific radioactivity of urinary purines increased in the control group from a mean of 1.29 X 10(5) to 3.64 X 10(5) cpm/mmol of purines (P less than .02) but decreased in the enzyme-deficient subjects from a mean of 1.66 X 10(5) to 1.38 X 10(5) cpm/mmol. To assess if the decrease in the specific activity of urinary purines was due to an elevated rate of de novo purine synthesis, two HGPRT-deficient patients were treated with allopurinol and adenine followed five days later by a fructose infusion. The administration of adenine increased the specific activity of urinary purines after the infusion of fructose from a mean baseline value of 1.05 X 10(5) to 1.42 X 10(5) cpm/mmol of purines.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2725279&dopt=Abstract
Cell Struct Funct. 1987 Oct;12(5):407-20.
Role of superoxide radicals in cytotoxic effects of Fe-NTA on cultured normal liver epithelial cells.
Yamada M, Okigaki T, Awai M.
Department of Pathology, Okayama University Medical School, Japan.
We studied the cytotoxic effects of ferric nitrilotriacetate (Fe-NTA) on normal rat liver epithelial cells (RL34) cultured in medium containing 10% fetal calf serum. Marked cytolysis was present in cells exposed to greater than or equal to 25 micrograms/ml iron of Fe-NTA, but not all the cells exposed to 50 micrograms/ml iron were lethally injured. The remaining cells showed anomalous growth, namely cell pile-up and aggregation. Superoxide dismutase inhibited this iron-induced cytotoxicity, whereas catalase, mannitol, dimethyl sulfoxide, and 1,4-diazabicyclo-[2.2.2.] octane did not. RL34 cells exposed to Fe-NTA actually produced a large amount of superoxide radicals (O2-.), whereas unexposed control cells produced none. Allopurinol inhibited O2-. production and prevented cell injury by Fe-NTA. These results show that the injury to cells produced by Fe-NTA depends on the generation of O2-., the source of which may be xanthine oxidase.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2824065&dopt=Abstract
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