Larval rearing and ontogeny of digestive enzyme activities in yellowfin seabream (Acanthopagrus latus, Houttuyn 1782).

The present research was conducted to provide insight into digestive larval capacity in Acanthopagrus latus larvae from hatching up to 30 days after hatching (DAH). Newly hatched larvae were stocked into six 300-L cylindrical polyethylene tanks at a density of larvae 50 larvae/L and reared by means of the green water system using Nannochloropsis oculata (0.5 × 106/mL). After mouth opening, larvae were fed with rotifers (5-16 individual/mL) from 2 to 20 DAH; then, Artemia nauplii (0.5-3.0 individuals/mL) were offered to larvae from 18 to 30 DAH, meanwhile a commercial microdiet was offered to larvae from 25 to 30 DAH. Larval performance in terms of growth and survival, and the assessment of the activity of selected digestive enzymes ontogeny of digestive enzymes activities was evaluated in larvae sampled at 0 (hatching), 7, 15, 22 and 30 DAH. Larvae showed an exponential growth characterized by two different growth stanzas, a first one characterized by slow growth rates comprised between hatching to 15 DAH (4.7 ± 0.2 mm), followed by a period of faster growth rates between 16 and 30 DAH (7.5 ± 0.6 mm). The activities of the brush border (alkaline phosphatase, ALP) and cytosolic (leucine-alanine peptidase, LAP) enzymes, as well as those of the pancreatic ones like total alkaline proteases, bile salt-activated lipase and α-amylase were detected from the mouth opening stage. Total activities of pancreatic and gastric enzymes increased with larval growth showing an enhancement of digestive capacities with larval age and size. The intestinal maturation in A. latus as assessed by the ratio of AP to LAP did not occur as expected by end of the first month of life suggesting the complete establishment of digestive luminal processes may take place at older ages. This study related to the growth patterns and ontogenic changes in activity of pancreatic, gastric and intestinal enzymes in A. latus and their nutritional regulation may be considered as the first step for improving the larviculture, as well as assessing and refining the nutritional requirements during the larval and early juvenile stages of this sparid species.

Neuroprotective Effects of Forced Exercise and Bupropion on Chronic Methamphetamine-induced Cognitive Impairment via Modulation of cAMP Response Element-binding Protein/Brain-derived Neurotrophic Factor Signaling Pathway, Oxidative Stress, and Inflammatory Biomarkers in Rats.

BACKGROUND: Forced exercise can act as non-pharmacologic neuroprotective agent. In current study, we tried the involved molecular mechanisms of protective effects of forced exercise against methamphetamine induced neurodegeneration. MATERIALS AND METHODS: Forty adult male rats were divided to Group 1 and 2 which received normal saline and methamphetamine (10 mg/kg) respectively for 30 days. Groups 3, 4 and 5 were treated with methamphetamine for first 15 days and then were treated by forced exercise, bupropion (20 mg/kg/day) or combination of them for the following 15 days. Between 26th and 30th days, Morris Water Maze (MWM) was used to evaluate the cognition. On day 31, hippocampus was isolated from each rat and oxidative, antioxidant and inflammatory factors also the level of total and phosphorylated forms of cAMP response element-binding protein (CREB) and brain derived neurotrophic factor (BDNF) proteins were also evaluated. RESULTS: Chronic abuse of methamphetamine could decreases cognition and increase malondialdehyde (MDA), Tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1ß), while caused decreases in superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GR) activities all these changes was significant (P < 0.001) in compared to control group while treatment with bupropion, forced exercise and bupropion in combination with forced exercise could prevent all these malicious effects of methamphetamine (P < 0.001). Bupropion, forced exercise and bupropion in combination with forced exercise could activate CREB (both forms) and activates BDNF proteins' expression with P < 0.001 in methamphetamine treated rats. CONCLUSIONS: P-CREB/BDNF signaling pathways might have critical role in forced exercise protective effects against methamphetamine induced neurodegeneration.