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PubMed1971

Egg proteins in cod serum. Natural occurrence and induction by injections of oestradiol 3-benzoate.

1. Before the uptake of water that precedes spawning, eggs of cod (Gadus morhua L.) contained 30% dry matter, of which 80% was protein. Some 75% of this protein was soluble in 0.5m-sodium chloride. The major components in the extract were two similar lipoproteins, of molecular weight about 400000, containing 21% lipid, some two-thirds of which was phospholipid, and about 0.5% protein phosphorus. 2. These lipoproteins were identified by immunochemical methods in the serum of female cod with developing ovaries, but not in the serum of male or of immature female fish. 3. The concentrations of egg proteins in the serum of female cod were determined by a serial-dilution double-diffusion immunological method, and were shown to increase with development of the ovaries, reaching a value of about 32mg/ml when the weight of the ovaries was 10% of the weight of the fish. 4. Immature male and female cod were injected intramuscularly with a solution of oestradiol-17beta 3-benzoate in oil and the concentration of egg proteins in their serum was measured by the immunodiffusion method. The serum contained no detectable egg proteins before injection of the fish, but 30mug of oestradiol benzoate/kg gave rise to detectable amounts of egg proteins in 10 days, and with 300mug or 1mg of oestradiol benzoate/kg the concentration of egg proteins rose to 32mg/ml. The values for male and female cod were similar and represented about one-half of the total serum protein. 5. With a dose of 1mg of oestradiol benzoate/kg, egg proteins were first detected in the serum 2 days after injection and the concentration increased up to 10 days. 6. Serum samples taken before and 10 days after an injection of 1mg of oestradiol benzoate/kg were fractionated by gel-filtration on Sephadex G-200. The difference curves obtained from fractionation curves after and before injection confirmed the values of the concentrations of egg proteins obtained from the immunodiffusion test and showed that the concentrations of the normal serum components fell by 20-50% of the initial value, the high-molecular-weight globulins showing the most marked fall. 7. Egg proteins were detected in the liver and testes of the injected fish, but not in the ovaries.

Animals↗

PubMed1994

n-3 fatty acids inhibit defects and fatty acid changes caused by phenytoin in early gestation in mice.

Our previous work has shown that n-3 fatty acids exert a protective effect against phenytoin-induced cleft palate when phenytoin was administered midgestation [gestational days (GD) 12 and 13] to CD-1 mice. The effects of dietary n-3 fatty acids on phenytoin teratogenicity were investigated at an earlier gestational period (GD 9) to examine whether n-3 fatty acids could exert protective action against other teratogenic effects of phenytoin apart from cleft palate. The effect of phenytoin exposure on maternal hepatic polyunsaturated fatty acid composition was also studied since delta 6 desaturase activity has been shown to be modified by pharmacological action. Female CD-1 mice were fed a standard laboratory diet (SLD), safflower oil (SAFF) or a cod liver/linseed oil (CLO/LO)-based diet for three weeks prior to impregnation and throughout pregnancy. Pregnant mice were administered a single i.p. dose of phenytoin on GD 9, and teratological assessments were performed on GD 19. Tissues were harvested on GD 10 for maternal hepatic phospholipid fatty acid analysis from another group of phenytoin-treated mice. The CLO/LO and the SLD mice, as compared to the SAFF-fed animals, showed a reduction in total malformations and fetal growth retardation due to phenytoin. Open eye defect was the only anomaly induced by phenytoin in the CLO/LO fetuses while phenytoin produced a variety of malformations in the SAFF fetuses such as tail defects, cleft palate, open eye and absence or blockage of the ureter.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormalities, Drug-Induced↗

PubMed2004

Effects of alkylphenols on redox status in first spawning Atlantic cod (Gadus morhua).

Offshore oil production releases large amounts of lipophilic compounds in produced water and into the ocean. The discharge of produced water from the Norwegian petroleum sector has increased from 26 million m3 in 1993 to 120 million m3 in 2001, and it continues to increase. Produced water contains significant amounts of alkylphenols, which have been reported to be estrogenic, causing endocrine disruption in fish. In year 2000, approximately 44 tons of alkylphenols were released on the Norwegian continental shelf in connection with discharge of produced water. Except from being estrogenic, relatively little is known about the effects of alkylphenols when released in the marine environment. Our objective was to study how alkylphenols affect the redox status in first spawning Atlantic cod (Gadus morhua) of both sexes. Model compounds tested included 4-tert-butylphenol (C4), 4-n-pentylphenol (C5), 4-n-hexylphenol (C6) and 4-n-heptylphenol (C7), all found in produced water. First spawning Atlantic cod were force-fed a mixture of these four alkylphenols, ranging between 0.02 and 80 ppm or 5 ppm 17beta-estradiol (E2), for 1 or 4 weeks. Increased hepatic total glutathione concentration in response to alkylphenol exposure was detected in female fish compared to control group after 1-week exposure, an effect not seen after 4 weeks. Furthermore, hepatic total glutathione concentration was sex dependent, where male fish sampled after 4 weeks had higher levels of glutathione than female fish. Increased glutathione reductase catalytic activities in both male and female fish were seen after exposure to 0.02 ppm alkylphenol mixture in 4 weeks. The glutathione S-transferase activity was only affected in male fish exposed to 0.02 ppm alkylphenols, and glucose-6-phosphate dehydrogenase activity increased in female fish exposed to 0.02 ppm alkylphenol mixture for 1 week. The increase of hepatic total glutathione content as well as the effects on glutathione reductase activities suggests that alkylphenol exposure affects the redox status in Atlantic cod.

Animals↗