Biochemical and histological studies of over-ripened oocyte in the Caspian brown trout (Salmo trutta caspius) to determine biomarkers for egg quality

The aims of the present study were to determine the best time for egg stripping after ovulation and to study oocyte over-ripening in the Caspian brown trout (Salmo trutta caspius). Eggs were retained in the female abdominal cavity for 40 days post ovulation (DPO). Partial volumes of eggs stripped from 10 individually identified females at 10 days intervals and fertilized with a pool of semen obtained from 8 males. The biochemistry and histology of the eggs and the biochemistry of the ovarian fluid were studied. The eyeing and hatching rate of the eggs declined with over-ripening time, which decreased from 90.60±6.28% for eyeing and 86.33±6.82% for hatching in newly ovulated eggs (0–10 DPO) to 1.34±0.67% for eyeing and 0.98±0.49% for hatching in over-ripened eggs (30–40 DPO). However, larval abnormalities remained constant for 30 days after ovulation. During the course of oocyte over-ripening, the pH of the ovarian fluid significantly decreased and the concentration of glucose, protein, calcium, iron, and aspartate aminotransferase activity significantly increased. Moreover, the concentration of protein, triglycerides, and aspartate aminotransferase activity in the eggs changed with over-ripening. In the newly ovulated eggs, the yolk consisted of homogenous tissue and its perivitelline space diameter had no considerable differences. With over-ripening, the yolk became heterogeneous, and while chorion diameter did not change, the perivitelline space diameter varied among different areas. The present study demonstrated that the best time to take Caspian brown trout eggs after ovulation at 7±0.6°C was up to 10 DPO. Among the studied parameters of the egg and ovarian fluid, egg quality was related to both ovarian fluid parameters (pH, protein, aspartate aminotransferase, glucose, cholesterol, triglycerides, calcium) and egg parameters (iron, aspartate aminotransferase), suggesting that these parameters can be used as egg quality biomarkers for Caspian brown trout

Proposed recommendations for diagnosing and managing individuals with glutaric aciduria type I: second revision

Glutaric aciduria type I (GA-I; synonym, glutaric acidemia type I) is a rare inherited metabolic disease caused by deficiency of glutaryl-CoA dehydrogenase located in the catabolic pathways of L-lysine, L-hydroxylysine, and L-tryptophan. The enzymatic defect results in elevated concentrations of glutaric acid, 3-hydroxyglutaric acid, glutaconic acid, and glutaryl carnitine in body tissues, which can be reliably detected by gas chromatography/mass spectrometry (organic acids) and tandem mass spectrometry (acylcarnitines). Most untreated individuals with GA-I experience acute encephalopathic crises during the first 6 years of life that are triggered by infectious diseases, febrile reaction to vaccinations, and surgery. These crises result in striatal injury and consequent dystonic movement disorder; thus, significant mortality and morbidity results. In some patients, neurologic disease may also develop without clinically apparent crises at any age. Neonatal screening for GA-I us being used in a growing number of countries worldwide and is cost effective. Metabolic treatment, consisting of low lysine diet, carnitine supplementation, and intensified emergency treatment during catabolism, is effective treatment and improves neurologic outcome in those individuals diagnosed early; treatment after symptom onset, however, is less effective. Dietary treatment is relaxed after age 6 years and should be supervised by specialized metabolic centers. The major aim of this second revision of proposed recommendations is to re-evaluate the previous recommendations (Kölker et al. J Inherit Metab Dis 30:5-22, 2007b; J Inherit Metab Dis 34:677-694, 2011) and add new research findings, relevant clinical aspects, and the perspective of affected individuals