Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.16.3.1 (ceruloplasmin)
 5,074 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Men who chronically abuse alcohol may display a spectrum of endocrine abnormalities including hypogonadism and feminization, with elevated serum estradiol and low serum testosterone. We examined factors that may result in disruption of hepatic sex hormone homeostasis in alcohol-fed male rats and possible consequences of such changes. Rats were fed alcohol-containing or isocaloric diets for 30, 60, and 90 days. In alcohol-fed rats, serum testosterone levels and hepatic activity of 2 androgen-dependent estrogen metabolizing enzymes were reduced (P <.05) at all times, as was activity of androgen receptor. There was also a significant early and progressive decrease in testes/body ratio in alcohol-fed rats. Compared with this early decrease in testosterone-related parameters, there was a significant increase in serum estrogen levels (at 30 and 90 days, 132% and 168% of control values, respectively). An increase in serum ceruloplasmin, an estrogen-responsive liver protein, was apparent at 60 and 90 days, but not at 30 days of alcohol exposure, suggesting that hypogonadism precedes liver feminization. Hepatic estrogen receptor activity was decreased in alcohol-fed rats at 60 and 90 days, the latter despite elevated serum estrogen levels. Hepatic aromatase was slightly increased in alcohol-fed rats, an elevation probably not sufficient to account for observed increases in serum estrogen. Taken together, these data suggest that (1) alcohol induces profound reduction of serum testosterone, resulting in loss of androgen-regulated hepatic functions such as estrogen-metabolizing enzyme activity and activity of androgen receptors; and (2) such alcohol-induced hypogonadism precedes changes in hepatic sex hormone homeostasis and subsequent feminization.
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PMID:Hypogonadism precedes liver feminization in chronic alcohol-fed male rats. 1079 90

The immunotoxicity of tributyltin (TBT) on marine gastropods has been comparatively little studied although risks to wildlife associated with this compound are well known. In this study, a 30-day trial was conducted to evaluate the immunotoxic effects on abalone (Haliotis diversicolor supertexta) by exposing a range of doses of TBT (0, 2, 10, and 50 ng/L). Innate immune parameters, including phagocytic ability (PA), lysozyme activity, phenoloxidase (PO) level and superoxide dismutase (SOD) activity were monitored at intervals of 5, 15 and 30 days. Haemolymph protein expression profile was also examined at the end of the experiment. The results showed that PA value, lysozyme activity and PO level significantly decreased compared with the controls (P < 0.05), which indicated that TBT exposure markedly suppressed non-specific immune competence. Exposure to TBT also caused variation in protein expression patterns of haemolymph. Among the protein spots of differential expressions, seven proteins from the haemolymph of TBT-treated abalone were successfully identified by MALDI-TOF-MS analysis. Three protein spots increased and were identified as carrier-like peptide, peroxidase 21 precursor and creatine phosphokinase. These proteins are believed to up-regulate in expression as a response to detoxification and antioxidative stress mechanisms. The other four protein spots that down-regulated in TBT-treated groups were identified as aromatase-like protein, protein kinase C, ceruloplasmin and microtubule-actin crosslinking factor 1, and these proteins play an important role in endocrine regulation and immune defense. Taken together, the results demonstrate that TBT impair abalone immunological ability and is a potential immune disruptor.
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PMID:Innate immune parameters and haemolymph protein expression profile to evaluate the immunotoxicity of tributyltin on abalone (Haliotis diversicolor supertexta). 2048 99

Wilson-Konovalov's disease (DWK) is a polysyndrome hereditary disease associated with excessive accumulation of copper due to the delay in its removal from the body. The condition of the reproductive system in patients with DWK is not well understood. It is proved that copper is a microelement necessary for the synthesis of estrogens, the secretion of prostaglandins in the endometrium. According to the results of the study, in reproductive age patients with DWK who do not receive adequate therapy, the reproductive function is impaired. Often amenorrhea, spontaneous abortions, infertility are noted. Violation of the reproductive function in this disease is associated primarily with liver failure and toxicity of copper. In the absence of treatment, copper, not bound by ceruloplasmin, penetrates from the plasma into the tissues, disrupting the function of the ovaries by reducing aromatase activity. At the heart of these disorders is the toxic effect of copper on the ovaries. Pregnancy in DWK is not contraindicated in the absence of liver failure and portal hypertension. During pregnancy, the negative balance of copper, in addition to adherence to diet and drug therapy, is supported by additional consumption of copper for the construction of fetal tissues, and subsequently for lactation. The onset of pregnancy is desirable only after the normalization of transaminase activity and the transition to the phase of maintenance therapy. Treatment should not stop; The risk of withdrawal of treatment during pregnancy is greater than the risk of continuing it. To date, sufficient experience has been accumulated in the treatment of d-penicillamine, trientine, zinc preparations during pregnancy and the absence of teratogenic action. The article presents a clinical case of a favorable outcome of pregnancy in (DWK). This example shows that the use of chelates and zinc salts in patients with (DWK) is associated with a positive pregnancy outcome for the mother and fetus.
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PMID:[A favorable outcome of pregnancy with Wilson-Konovalov disease (a clinical case)]. 3017 51