Arachidonic Acid Supplementation Research Articles

Developmental docosahexaenoic and arachidonic acid supplementation improves adult learning and increases resistance against excitotoxicity in the brain

Through metabolic imprinting mechanisms a number of bioactive molecules including polyunsaturated fatty acids affect brain functions in the developmental age and longer-lasting beneficial effects are expected. In this study pregnant rats were offered diets either containing no docosahexaenoic acid (DHA) and arachidonic acid (AA) (Placebo diet) or an excess amount of these long chain polyunsaturated fatty acids (LC-PUFA) (Supplement diet) up to the time of weaning. Bilateral N-methyl-D-aspartate (NMDA) induced neurodegeneration in the entorhinal cortex of offspring in the age of 4 months was used as a tool to investigate the neuroprotective property of the developmentally supplemented DHA and AA treatments. Hippocampus-dependent spatial learning was measured in Morris water maze and the extent of neuronal lesion in the injected brain area was evaluated. Under baseline condition, in intact or sham-lesioned rats, the Morris water maze performance was superior in the supplemented group compared to the placebo controls. NMDA-lesion in the entorhinal cortex area decreased spatial learning in the supplement-treated rats while insignificantly diminished it in the placebo controls. The same supplementation attenuated the lesion size induced by the NMDA injection into the entorhinal and ventral hippocampal areas. We concluded that LC-PUFA supplementation during fetal and early postnatal development results in long-term enhancement of spatial learning ability of the offspring and offers resistance against excitotoxic brain lesion which lasts up to the adult age.

Arachidonic acid supplementation does not affect N-methyl-N-nitrosourea-induced renal preneoplastic lesions in young Lewis rats

Arachidonic acid (AA) is naturally found in human breast milk. AA, together with docosahexaenoic acid, is commonly added as a functional food ingredient to commercial infant formula worldwide, in accordance with the international standards of Codex Alimentarius. However, few studies of the possible renal carcinogenic effects of AA supplementation during neonatal life have been performed. The effect of dietary AA supplementation in dams during gestation and lactation was investigated on N-methyl-N-nitrosourea (MNU)-induced preneoplastic lesions in the kidneys of young Lewis rats. Dams were fed a 2.0% AA diet or a basal diet (<0.01% AA). At birth (postnatal day 0), male and female pups received a single intraperitoneal injection of 35 mg/kg MNU or vehicle. Renal morphology was examined after 7, 14, 21, 28 and 60 days. Histopathologically, renal preneoplastic lesions, such as nephroblastomatosis and mesenchymal cell proliferation, were found on day 60 in both the MNU-treated groups. There was no significant difference in lesion incidence of 38% in the basal diet group and 31% in the AA diet group. In conclusion, an AA-rich diet for dams during gestation and lactation does not modify MNU-induced renal preneoplastic lesions in their offspring.

Fads2ノックアウトマウスによるアラキドン酸とドコサヘキサエン酸の新機能の発見

In mammals, arachidonic acid (ARA) and docosahexaenoic acid (DHA) play important physiological roles as precursors of eicosanoids and docosanoids, respectively. However, a full scope of the function of these fatty acids is yet to be elucidated. A major obstacle is endogenous synthesis of ARA and DHA from precursors. It is not possible to create ARA deficiency by dietary manipulation without depleting linoleic acid, which is an essential component of skin ceramides. Also, DHA deficiency cannot be created without a compensatory increase in 22:5 n-6. To overcome these obstacles, mice lacking the Fads2 gene that encodes the first step of ARA and DHA synthesis were created. When Fads2-null mice were fed a diet lacking ARA and DHA but containing sufficient linoleic and alpha-linolenic acid, they exhibited previously undocumented phenotypes. The Fads2-null mice developed ulcerative dermatitis after 4 months of age, which was distinct from dry, scaly dermatitis observed in classic linoleic acid deficiency. Fads2-null males exhibited complete arrest of sperm development at the stage of acrosome biogenesis. Intestinal ulcer was observed at duodenum and the ileo-cecal junction. In liver, lipid droplets were primarily localized in a periportal area. Dietary ARA prevented dermatitis and intestinal ulcer, whereas dietary DHA was ineffective. The male fertility and sperm formation were fully recovered by dietary DHA, whereas ARA was only partially effective. Either ARA or DHA supplementation prevented fatty liver. Although some of these phenotypes are likely due to reduced eicosanoid formation, the exact mechanism is yet to be elucidated.

アラキドン酸補給の安全性に関する研究

アラキドン酸補給の安全性に関する研究

An update on adding docosahexaenoic acid (DHA) and arachidonic acid (AA) to baby formula

Human milk is the ideal food providing optimal nutrition for healthy term infants. Its complex lipid composition is critical for infant growth and serves as a golden standard for baby formula development. Docosahexaenoic acid (C22:6 n- 3, DHA) and arachidonic acid (C20:4 n- 6, AA) are the two major long chain polyunsaturated fatty acids (PUFAs) in human milk. In humans, they are fundamental components of the cell membrane and play an important role in neurite growth and signal transmission. Their importance for both preterm and term infants has been demonstrated by various clinical trials. DHA and AA supplementation shows desirable influences on visual and cognitive development in early life and is additionally associated with potential benefits on later health. Further clinical data revealed that supplementing both DHA and AA instead of DHA alone during infancy is important to deliver the optimal outcome. In this review, we summarize current research and scientific evidence of DHA and AA on baby development.

Arachidonic acid supplementation during gestational, lactational and post-weaning periods prevents retinal degeneration induced by N-methyl-N-nitrosourea in young Lewis rats

Arachidonic acid supplementation during gestational, lactational and post-weaning periods prevents retinal degeneration induced by N-methyl-N-nitrosourea in young Lewis rats

Promoting effect of arachidonic acid supplementation on N-methyl-N-nitrosourea-induced pancreatic acinar cell hyperplasia in young Lewis rats.

Arachidonic acid (AA) is naturally found in human breast milk. AA, together with docosahexaenoic acid, is commonly added as a functional food ingredient to commercial infant formula worldwide, in accordance with the international standard of Codex Alimentarius. However, few studies have been performed that are concerned with the possible carcinogenic effects of AA supplementation during neonatal life. The effect of dietary AA supplementation in dams, during gestation and lactation, was investigated in N-methyl-N-nitrosourea (MNU)-induced preneoplastic lesions in the exocrine pancreas of young Lewis rats. Dams were fed either an AA (2.0% AA) or a basal (<0.01% AA) diet. On postnatal day 0 (at birth), male and female pups received a single intraperitoneal injection of either 35 mg/kg MNU or vehicle. The morphology and proliferating activity of the exocrine pancreas were examined by proliferative cell nuclear antigen immunohistochemistry 7, 14, 21, 28 and/or 60 days post-MNU. Histopathologically, acinar cell hyperplasia (ACH) occurred in the MNU-treated groups 60 days after MNU injection, irrespecitive of whether the rats had been fed an AA diet. Morphometrically, the number and area of ACH per 1 mm(2) in MNU-treated rats increased significantly in the AA diet-fed rats, compared with basal diet-fed rats. The number of proliferative cell nuclear antigen-positive acinar cells in both the normal and hyperplastic areas of MNU-treated rats increased significantly in the AA diet-fed rats. In conclusion, providing dams with an AA-rich diet during gestation and lactation promotes MNU-induced pancreatic ACH in young Lewis rats.

Arachidonic acid supplementation enhances in vitro skeletal muscle cell growth via a COX-2-dependent pathway

Arachidonic acid (AA) is the metabolic precursor to a diverse range of downstream bioactive lipid mediators. A positive or negative influence of individual eicosanoid species [e.g., prostaglandins (PGs), leukotrienes, and hydroxyeicosatetraenoic acids] has been implicated in skeletal muscle cell growth and development. The collective role of AA-derived metabolites in physiological states of skeletal muscle growth/atrophy remains unclear. The present study aimed to determine the direct effect of free AA supplementation and subsequent eicosanoid biosynthesis on skeletal myocyte growth in vitro. C2C12 (mouse) skeletal myocytes induced to differentiate with supplemental AA exhibited dose-dependent increases in the size, myonuclear content, and protein accretion of developing myotubes, independent of changes in cell density or the rate/extent of myogenic differentiation. Nonselective (indomethacin) or cyclooxygenase 2 (COX-2)-selective (NS-398) nonsteroidal anti-inflammatory drugs blunted basal myogenesis, an effect that was amplified in the presence of supplemental free AA substrate. The stimulatory effects of AA persisted in preexisting myotubes via a COX-2-dependent (NS-389-sensitive) pathway, specifically implying dependency on downstream PG biosynthesis. AA-stimulated growth was associated with markedly increased secretion of PGF(2α) and PGE(2); however, incubation of myocytes with PG-rich conditioned medium failed to mimic the effects of direct AA supplementation. In vitro AA supplementation stimulates PG release and skeletal muscle cell hypertrophy via a COX-2-dependent pathway.

Arachidonic acid supplementation during gestational, lactational and post-weaning periods prevents retinal degeneration induced in a rodent model

Fatty acids and their derivatives play a role in the response to retinal injury. The effects of dietary arachidonic acid (AA) supplementation on N-methyl-N-nitrosourea (MNU)-induced retinal degeneration was investigated in young Lewis rats during the gestational, lactational and post-weaning periods. Dams were fed 0·1, 0·5 or 2·0% AA diets or a basal (< 0·01% AA) diet. On postnatal day 21 (at weaning), male pups received a single intraperitoneal injection of 50 mg MNU/kg or vehicle, and were fed the same diet as their mother for 7 d. Retinal apoptosis was analysed by the terminal deoxynucleotidyl transferase-mediated dUTP digoxigenin nick-end labelling (TUNEL) assay 24 h after the MNU treatment, and retinal morphology was examined 7 d post-MNU. Histologically, all rats that received MNU and were fed the basal and 0·1% AA diets developed retinal degeneration characterised by the loss of photoreceptor cells (disappearance of the outer nuclear layer and the photoreceptor layer) in the central retina. The 0·5 and 2·0% AA diets rescued rats from retinal damage. Morphometrically, in parallel with the AA dose (0·5 and 2·0% AA), the photoreceptor ratio significantly increased and the retinal damage ratio decreased in the central retina, compared with the corresponding ratios in basal diet-fed rats. In parallel with the increase in serum and retinal AA levels and the AA:DHA ratio, the apoptotic index in the central retina was dose-dependently decreased in rats fed the 0·5 and 2·0% AA diets. In conclusion, an AA-rich diet during the gestation, lactation and post-weaning periods rescued young Lewis rats from MNU-induced retinal degeneration via the inhibition of photoreceptor apoptosis. Therefore, an AA-enriched diet in the prenatal and postnatal periods may be an important strategy to suppress the degree of photoreceptor injury in humans.

Dietary Long-Chain PUFA Enhance Acute Repair of Ischemia-Injured Intestine of Suckling Pigs1–3

Infant formula companies have been fortifying formulas with long-chain PUFA for 10 y. Long-chain PUFA are precursors of prostanoids, which stimulate recovery of intestinal barrier function. Supplementation of milk with PUFA increases the content of arachidonic acid (ARA) in enterocyte membranes; however, the effect of this enrichment on intestinal repair is not known. The objective of these experiments was to investigate the effect of supplemental ARA on intestinal barrier repair in ischemia-injured porcine ileum. One-day-old pigs (n= 24) were fed a milk-based formula for 10 d. Diets contained no PUFA (0% ARA), 0.5% ARA, 5% ARA, or 5% EPA of total fatty acids. Following dietary enrichment, ilea were subjected to in vivo ischemic injury by clamping the local mesenteric blood supply for 45 min. Following the ischemic period, control (nonischemic) and ischemic loops were mounted on Ussing chambers. Transepithelial electrical resistance (TER) was measured over a 240-min recovery period. Ischemia-injured ileum from piglets fed 5% ARA (61.0 ± 14%) exhibited enhanced recovery compared with 0% ARA (16 ± 14) and 0.5% ARA (22.1 ± 14)-fed pigs. Additionally, ischemia-injured ileum from 5% EPA (51.3 ± 14)-fed pigs had enhanced recovery compared with 0% ARA-fed pigs (P< 0.05). The enhanced TER recovery response observed with ischemia-injured 5% ARA supplementation was supported by a significant reduction in mucosal-to-serosal flux of3H-mannitol and14C-inulin compared with all other ischemia-injured dietary groups (P< 0.05). A histological evaluation of ischemic ilea from piglets fed the 5% ARA showed reduced histological lesions after ischemia compared with the other dietary groups (P< 0.05). These data demonstrate that feeding elevated levels of long-chain PUFA enhances acute recovery of ischemia-injured porcine ileum.

Omega-3 fatty acids cause dramatic changes in TLR4 and purinergic eicosanoid signaling

Dietary fish oil containing ω3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), elicit cardioprotective and anti-inflammatory effects through unresolved mechanisms that may involve competition and inhibition at multiple levels. Here, we report the effects of arachidonic acid (AA), EPA, and DHA supplementation on membrane incorporation, phospholipase A(2) catalyzed release, and eicosanoid production in RAW264.7 macrophages. Using a targeted lipidomics approach, we observed that Toll-like receptor 4 and purinergic receptor activation of supplemented cells leads to the release of 22-carbon fatty acids that potently inhibit cyclooxygenase pathways. This inhibition was able to shunt metabolism of AA to lipoxygenase pathways, augmenting leukotriene and other lipoxygenase mediator synthesis. In resident peritoneal macrophages, docosapentaenoic acid (DPA) was responsible for cyclooxygenase inhibition after EPA supplementation, offering fresh insights into how EPA exerts anti-inflammatory effects indirectly through elongation to 22-carbon DPA.

Effect of Arachidonic Acid-enriched Oil Diet Supplementation on the Taste of Broiler Meat.

To elucidate the relationship between the arachidonic acid (AA) content and the taste of broiler meat, the effects of AA-enriched oil (AAO) supplements on the fatty acid content and sensory perceptions of thigh meat were evaluated. Four types of oil, including corn oil (CO), a 1:1 mixture of AAO and palm oil (PO) (1/2 AAO), a 1:3 mixture of AAO and PO (1/4 AAO), and a 1:7 mixture of AAO and PO (1/8 AAO) were prepared. Each type of oil was mixed with silicate at a ratio of 7:3, and added to the diet at a final proportion of 5% of fresh matter. Broiler chickens were fed these diets for 1 wk before slaughter. In thigh meat, the AA content of the 1/2 and 1/4 AAO groups was significantly higher than that of the CO group. The AA content in thigh meat (y, mg/g) increased linearly with increasing dietary AAO content (x, g/100 g of diet), according to the equation y = 0.5674+0.4596× (r2 = 0.8454). The content of other fatty acids was not significantly different among the 4 diet groups. Sensory evaluation showed that the flavor intensity, umami (L-glutamate taste), kokumi (continuity, mouthfulness, and thickness), and aftertaste of the 1/2 and 1/4 AAO groups were significantly higher than that of the CO group. There were significant positive correlations between AA content in thigh meat and the flavor intensity, total taste intensity, umami, and aftertaste. These data suggest that the taste of broiler meat can be improved by the amount of dietary AA supplementation.

Omega‐3 Fatty Acids Cause Dramatic Changes in TLR‐4 and Purinergic Eicosanoid Signaling in Macrophages

Dietary fish oil omega‐3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), elicit cardioprotective and anti‐inflammatory effects through unresolved mechanisms. EPA and DHA may reduce arachidonic acid (AA) metabolism and pro‐inflammatory effects by competition and inhibition at multiple levels. Here, we report the effects of AA, EPA, and DHA supplementation on membrane incorporation, phospholipase A2 release, and eicosanoid production in RAW264.7 macrophages. Each PUFA supplemented increased by similar amounts in membrane phospholipids, while half of the increased AA and EPA were elongated to adrenic acid (AdA) and docosapentaenoic acid (DPA), respectively; and were subsequently released by PLA2 at levels comparable to AA. TLR‐4 stimulated COX‐2 AA production did not increase with AA supplementation and was inhibited by 20% and 50% after EPA and DHA supplementation, respectively. ATP stimulated COX‐1 AA production was inhibited to a greater extent by EPA and DHA; 5‐LOX AA metabolites increased 2‐fold with EPA and DHA supplementation, and 5‐LOX metabolized EPA and DHA to a greater extent than COX‐1/COX‐2. Altogether, AA, EPA and DHA supplementation decreased TLR‐4 stimulated AA COX‐2 prostanoid metabolism; increased the purinergic stimulated AA 5‐LOX/COX‐1 ratio; and significantly increased elongated PUFA levels that may be converted to novel mediators.

Supplemental arachidonic acid-enriched oil improves the taste of thigh meat of Hinai-jidori chickens

The Hinai-dori is a breed of chicken native to the Akita prefecture in Japan. A cross between the Hinai-dori and Rhode Island Red breeds has been commercialized as the Hinai-jidori chicken, one of the most popular brands in Japan. High arachidonic acid (AA) content is a characteristic feature of Hinai-jidori chicken meat. To elucidate the relationship between AA content and the palatability of the Hinai-jidori chicken, we examined the effects of palm oil (PO), corn oil (CO), and arachidonic acid-enriched oil (AAO) diet supplementation on the fatty acid content and sensory perceptions in thigh meat. Each oil and silicate was mixed at a ratio of 7:3, 5% of fresh matter was added to the finisher diet, and Hinai-jidori chickens were fed these diets for 2 wk before slaughter. In thigh meat, the AA content of the AAO group was significantly more than 2-fold higher than that of the PO and CO groups. Other fatty acid contents were not significantly different among the groups. Sensory evaluation showed that the total taste intensity, umami (l-glutamate taste), kokumi (continuity, mouthfulness, and thickness), and aftertaste of the AAO group were significantly higher than those of PO and CO groups in both chicken soup and steamed minced meat. These data suggest that the palatability of chicken meat can be improved by dietary AA supplementation.

Effects of n-6 polyunsaturated fatty acids on prostaglandin production in ovine fetal chorion cells in vitro in late gestation ewes

Objective To use an in vitro model of the ovine placenta to determine effects of n-6 polyunsaturated fatty acid (PUFA) supplementation on prostaglandin (PG) production. PGs are key regulators of fetal maturation and parturition. Study design Fetal allantochorion tissue (FC) was collected in late pregnancy (day 135). FC cells were isolated and cultured with 0–100 μM of linoleic acid (LA), γ-linolenic acid (GLA) or arachidonic acid (AA) in serum free medium and challenged with control medium, lipopolysaccharide (LPS, 0.1 μg/ml), dexamethasone (DEX, 5 μM) or a combination of LPS (0.1 μg/ml) with DEX (5 μM). Spent medium was harvested at 2 h and 24 h post challenge for measuring PGs. Main outcome measures To assess the effects of treatment on placental 1- and 2-series PGE production. Results LA supplementation inhibited both PGE 1 and PGE 2 production. GLA predominantly stimulated PGE 1 generation, although it also increased PGE 2 production. AA supplementation predominantly increased PGE 2 production, but also stimulated PGE 1. DEX treatment with or without LPS inhibited PG production. Supplementation with n-6 PUFAs attenuated or neutralised the stimulatory effect of LPS challenge on FC cells for both PGE 1 and PGE 2 production. Conclusion These data show that supplementation with n-6 PUFAs alters placental PG production, but their precise effects depend on their position in the biosynthetic pathway for PG synthesis. This study supports the possibility that GLA containing oils, widely promoted as dietary supplements, might reduce the risk of pre-term labour by inhibiting the responsiveness of PGE 2 production to LPS challenge in the placenta.

Effects of dietary arachidonic acid on larval performance, fatty acid profiles, stress resistance, and expression of Na +/K + ATPase mRNA in black sea bass Centropristis striata

Dietary arachidonic acid (ARA, 20:4n-6) supplementation on larval performance, tissue fatty acid profiles, resistance to hypersaline stress and expression of Na +/K + ATPase mRNA was studied in black sea bass Centropristis striata from the first feeding through metamorphosis at 24 days post-hatching (d24ph). Thirty 15-L aquaria were stocked with d1ph yolksac stage larvae at 100 ind/L. Salinity (34 g/L), temperature (22 °C), photoperiod (18L:6D), light intensity (1000 lx), diffused aeration (100 mL/min) and D.O. (> 5 mg/L) were held constant. Non-viable microalgae Nannochloropsis oculata was maintained at 300,000 cells/mL as background. To evaluate the effects of dietary arachidonic acid (ARA) supplementation, live prey, rotifers Brachionus rotundiformis and Artemia sp., was enriched with emulsions containing 10% docosahexaenoic acid (DHA, 22:6n-3) and five different levels of ARA (0, 6, 8, 10 and 12% total fatty acids, TFA). In a sixth treatment, live prey was enriched with a premium commercial fatty acid booster (26% DHA, 0% ARA). Rotifers were fed from d2 to d20ph at 10–23 ind/mL, while Artemia were fed from d18 to d22ph at 0.5–3 ind/mL. On d24ph, larval fatty acid profiles reflected dietary levels, and no significant (P > 0.05) differences in larval growth (notochord length, wet and dry wt.), survival (range = 24.3–32.7%), or hypersaline stress resistance (ST-50 = 27.1–31.8 min) among treatments were evident. However, larvae fed diets supplemented with ARA (6–12% TFA) demonstrated a significant (P < 0.05) increase in Na +/K + ATPase mRNA 24 h after a sublethal salinity (43 g/L) challenge, whereas larvae fed 0% ARA and the commercial diet (devoid of ARA) showed no significant increase. The results suggested that dietary supplementation with ARA at 6–12% promoted the adaptive physiological responses to hypersalinity stress and hypo-osmoregulatory ability in black sea bass larvae.

Essential fatty acid supplementation of DHA and ARA and effects on neurodevelopment across animal species: a review of the literature

Docosahexanoic acid (DHA) and arachidonic acid (ARA) are long chain essential fatty acids used as supplements in commercial infant formula. DHA/ARA deficient states are associated with adverse neurological outcomes in animals and humans. Preterm infants are at risk for DHA/ARA deficiency. A few clinical reports on the effects of fatty acid supplementation have shown benefit in preterm, low birth weight, and normal infants in the first year of life, whereas others did not. Studies in animals have reported shortened gestation, fetal growth retardation, reduced infant body mass, and increased fetal mortality with consumption of fatty acids during pregnancy. To understand the data that support fatty acid supplementation in infant formula, a review of the animal model literature was undertaken, to examine the effects of DHA/ARA on neurodevelopment, including the effects on visual acuity. Several points emerged from this review. (1) Animal studies indicate that requirements for DHA/ARA vary depending on developmental age. Alterations of the ratio of DHA/ARA can impact developmental outcome. (2) The available studies suggest that while supplementation of DHA/ARA in an appropriate ratio can increase tissue levels of these fatty acids in the brain and retina, tissues sensitive to depletion of fatty acids, the benefit of routine supplementation remains unclear. Few studies measure functional outcome relative to changes in physiologic pools of DHA/ARA after supplementation. (3) Animal literature does not support a clear long-term benefit of replenishing DHA/ARA tissue levels and administration of these fatty acids at concentrations above those in human milk suggests adverse effects on growth, survival, and neurodevelopment.

The influence of dietary supplementation of arachidonic acid on prostaglandin production and oxidative stress in the Pacific oyster Crassostrea gigas

In a previous study, dietary supplementation with arachidonic acid (ARA) to oysters Crassostrea gigas increased haemocyte numbers, phagocytosis, and production of reactive oxygen species level (ROS) by haemocytes ( Delaporte et al., 2006). To assess if the observed stimulation of these cellular responses resulted from changes of ARA-related prostaglandin (PG) production, we analysed prostaglandin E2 metabolite (PGEM) content on the same oysters fed three levels of ARA. Dietary supply of polyunsaturated fatty acids (PUFA) could also induce an oxidative stress that could similarly increase cellular responses; therefore, two indicators of oxidative stress were analysed: peroxidation level and antioxidant defence status. Together the observed positive correlation between ARA and PGEM levels and the absence of lipid peroxidation and antioxidant activity changes supports the hypothesis of an immune stimulation via PG synthesis. Although ARA proportion in oyster tissues increased by up to 7-fold in response to ARA dietary supplementation, peroxidation index did not change because of a compensatory decrease in n-3 fatty acid proportion, mainly 22:6n-3. To further confirm the involvement of PG in the changes of haemocyte count, phagocytosis and ROS production upon ARA supplementation, it would be interesting to test cyclooxygenase and lipooxygenase inhibitors in similar experiments.

Maternal arachidonic acid and iron supplementation improves performance in Morris Water Maze in 28‐day old offspring from diabetic rats – a pilot study

Maternal arachidonic acid and iron supplementation improves performance in Morris Water Maze in 28‐day old offspring from diabetic rats – a pilot study

Effect of lipid supplementation on reproductive performance of female channel catfish, Ictalurus punctatus, induced and strip-spawned for hybridization

The influence of different lipid sources and n3:n6 ratios on reproductive performance of female channel catfish, Ictalurus punctatus was evaluated. A commercial catfish feed was top coated with 2% oil and offered to brood stock females fish during 70–85 days before spawning season. Four dietary treatments were formulated using the following top coating ratios: diet 1, soybean oil 9.5 g kg−1 and linseed oil 10.5 g kg−1; diet 2, soybean oil 17.5 g kg−1 and linseed oil 2.5 g kg−1; diet 3, 20.0 g kg−1 linseed oil, and diet 4, 10.0 g kg−1 menhaden fish oil, supplemented with 5.0 g kg−1 arachidonic acid (ARA), and 5.0 g kg−1 docosahexaenoic acid (DHA). Fatty acid composition of the eggs reflected the effect of dietary treatment offered during spring season. Supplementation of ARA, EPA and DHA in commercial catfish feed in the form of menhaden fish oil with purified liquid algae extracts of ARA and DHA produced from two to five times the number of fry per female body weight when compared to the effect of fed top coated with vegetable oils. Although, this effect was not statistically significant it may represent an economical improvement for the industry.