No abstract

The purpose of this study was to investigate the effect of freshwater rearing on the fatty acid profiles of the whole body and muscle tissue of the European sea bass (Dicentrarchus labrax). Half of initial fish were gradually acclimated to freshwater (FW) kept at the same temperature to salt water and grown in same conditions as their counterparts in saltwater (SW). The decrease in salinity caused an increase in the percentages of 18:1n -9, 24:1n -9, 18:3n -3, 18:2n -6 and decrease in the percentages of 14:0, 15:0, 20:0, 21:0, 20:5n -3 and 22:6n -3 both in the whole body and in the muscle tissue fatty acid profiles. The lipids of FW-reared fish contained significantly (P \ 0.01) higher percentages of 18:2n -6 and 18:3n -6 than that of SW-reared fish. However, percentages of 20:5n -3 and 22:6n -3 fatty acids decreased significantly (P \ 0.05) compared with those of salt water-reared European sea bass. There was a clear trend of decrement in the percentages of n -3 PUFA fatty acids due to the decrease in water salinity. However, the percentages of n -6 PUFA fatty acids were also increased with the decrease in water salinity. We concluded that the FW acclimation is followed by changes in certain lipid classes of sea bass muscle tissue and whole body samples. n -3/n -6 PUFA ratios were characteristic to previously reported ratios for both FW-and SW-reared European sea bass. In addition, EPA/DHA ratios were basically similar for the fish reared in both SW and FW indicating the equal nutritional value of the final products in terms of providing PUFA's for human nutrition.

Immobilization for 2 h significantly decreased plasma concentrations of 13 of 16 amino acids assayed, including the transmitter amine precursors tyrosine and total tryptophan. The level of plasma free tryptophan, however, was increased. Despite the reduced plasma levels, corresponding brain concentrations of many large neutral amino acids (LNAAs) were increased (tryptophan, phenylalanine, valine, leucine, and isoleucine). Brain concentrations of tyrosine and the other amino acids measured were unaltered. The results for the LNAAs were not explained by calculated brain influx rates. Therefore, altered influx kinetics or perhaps altered brain protein metabolism or efflux may be responsible. Comparison of calculated brain influxes and brain concentrations of LNAAs suggests that the rise in level of plasma free tryptophan during immobilization is not responsible for the increase in level of brain tryptophan and that the mechanism responsible for the maintenance of or increase in brain concentrations of the other LNAAs is probably involved. Maintenance of brain concentrations of basic amino acids is explicable by reduced competition for brain uptake.

Ability of ascorbic acid (vitamin C) to attenuate oxidative damage was evaluated in liver and brain tissues of Oreochromis niloticus (O. niloticus) experimentally exposed to sublethal concentrations of chlorpyrifos (CPF). O. niloticus was exposed to sublethal concentrations of CPF at 12 μg/L (CPF1) and 24 μg/L (CPF2) for 96 h. The fish of vitamin C (Vit C) and CPF2 + Vit C groups were fed with Vit C supplemented diet (200 mg Vit C/100 g feed). A significant increase in thiobarbituric acid-reactive substances (TBARS) level (P < 0.05) was observed in brain of CPF-exposed fish although liver TBARS level was not changed compared to control group. This result showed that lipid peroxidation (LPO) was elevated in brain of fish exposed to CPF. Glutathione peroxidase (GSH-Px) activity in liver and brain tissues was significantly elevated (P < 0.05) by exposure to CPF1 and CPF2. Catalase (CAT) activity was significantly increased (P < 0.05) in liver but decreased in brain of treated fish by CPF2 concentration. Superoxide dismutase (SOD) activity was decreased in liver, but increased in brain by exposure to CPF1 and CPF2 concentrations. Levels of TBARS were increased in brain of CPF-treated animals, but tended to decrease by the effect of Vit C. Vit C treatment for CPF-intoxicated animals normalized the otherwise raised activities of GSH-Px, CAT, and SOD within normal limits. The results clearly indicate that exposure to CPF caused a dose-dependent increase in oxidative stress brain and to a lesser extend in liver of fish and the ability of Vit C to attenuate CPF-induced oxidative damage.

Psychiatric patients undergoing the psychosurgical operation of stereotactic subcaudate tractotomy were infused intravenously with either saline or L-tryptophan (15 mg/kg/h). Plasma, lumbar cerebrospinal fluid (CSF), ventricular CSF and a specimen of frontal cortex were collected. The relationships of plasma concentrations of substances claimed to influence brain tryptophan concentration (total tryptophan, free tryptophan, large neutral amino acids) with the concentration of tryptophan in the cortex and CSF were investigated. Tryptophan infusion resulted in plasma tryptophan values comparable to those found after oral doses used in treating depression or insomnia, and about sixfold increases of tryptophan in the cerebral cortex. Increased brain 5-hydroxytryptamine synthesis was indicated by significant rises of CSF 5-hydroxyindoleacetic acid. The concentration of plasma free tryptophan was a better predictor than plasma total tryptophan of cortex tryptophan concentration. As all correlation coefficients of plasma versus brain or plasma versus ventricular CSF tryptophan concentrations were decreased when allowance was made for differences of concentration of large neutral amino acids, the results suggest that the role of these substances within their physiological range as inhibitors of tryptophan transport to the brain may previously have been overemphasised.