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Biomedical subjects

R E Anderson

Publications and source records attributed to R E Anderson.

At least 91 records · Page 5Linked to original sources
PubMed1998

Phospholipase Cgamma1 in bovine rod outer segments: immunolocalization and light-dependent binding to membranes.

We have investigated the isozymes of a phosphoinositide-specific phospholipase C (PLC) in bovine retina using several monoclonal antisera to PLCbeta1, gamma1, and delta1. Immunoblot analysis showed that all three isozymes were present in the retina. Immunocytochemical localization in frozen bovine retina sections showed that PLCgamma1 was present in the photoreceptor cell layer, outer plexiform cell layer, inner plexiform cell layer, and ganglion cell layer. Immunoreaction within the photoreceptor cell layer was dependent on dark/light adaptation state of retinas. Immunoblot analysis of rod outer segments (ROS) with monoclonal or polyclonal antibodies to PLCgamma1 showed the presence of an immunoreactive band of 140 kDa. ROS prepared from retinas light-adapted in vitro had more PLCgamma1 on immunoblots than ROS from dark-adapted retinas. PLC enzyme activity in ROS from light-adapted retinas was 69 and 46% higher than ROS from dark-adapted retinas, when assayed in the presence and absence of ATP, respectively. This increase in enzyme activity was observed at [Ca2+]free between 0.32 and 100 microM. These results demonstrate the presence of PLCgamma1 in bovine ROS and show that ROS prepared from light-adapted retinas are enriched in this isozyme, suggesting that light may promote the binding of this isozyme to bleached ROS membranes.

Adaptation, Ocular↗
PubMed1998

Regulation of n-3 and n-6 fatty acid metabolism in retinal and cerebral microvascular endothelial cells by high glucose.

The present study was undertaken to determine whether polyunsaturated fatty acid metabolism is affected by high glucose levels in cerebral and retinal microvascular endothelial cells. The metabolism of [3-14C]22:5n-3 and [1-14C]18:2n-6 was studied in cells previously cultured for 5 days in normal (5 mM) or high (30 mM) glucose medium. After incubation of retinal endothelial cells with [3-14C]22:5n-3 in the high glucose condition, the formation of labeled 24:6n-3 and 22:6n-3 was increased, and that of labeled 24:5n-3 was decreased, compared with the normal glucose condition. The changes were found for fatty acids esterified in cellular lipids and those released into the medium. After incubation with [1-14C]18:2n-6, levels of all elongation/desaturation products were increased at the expense of the precursor in retinal endothelial cells cultured in high glucose medium. The changes were primarily found for esterified fatty acids, with the release of n-6 fatty acids being minor in both glucose concentrations. By contrast, high glucose levels did not affect the metabolism of [3-14C]22:5n-3 and [1-14C]18:2n-6 in cerebral endothelial cells. The changes in metabolic activity of retinal endothelial cells were not reflected in the fatty acid composition. The present data suggest that high glucose can increase the desaturation process in retinal but not cerebral endothelial cells. This may produce some lipid abnormalities in retinal microvasculature and contribute to altered vascular function observed in diabetic retinopathy.

Animals↗
PubMed1998

Myocardial perfusion after coronary artery bypass surgery. A study using ectomographic myocardial scintigraphy and adenosine provocation.

A study was conducted to determine the time dependency of myocardial perfusion improvement after coronary artery bypass graft (CABG) surgery. Seventeen 3-vessel diseased patients (16 male, 1 female) scheduled for CABG surgery from a cardiac surgical and intensive-care unit were examined. Ten of the 17 patients returned for examination after 1 year. A titrated adenosine infusion was used to expose reversible ischemia. Tc99m-sestamibi was injected at rest and at maximum adenosine infusion rate, and isotope distribution was determined using ectomographic myocardial scintigraphy. Visually scored percent isotope uptake defect size and percent uptake reduction were assessed. It was found that resting isotope uptake defects were unchanged 1 h after surgery, increased in severity after 1 week, and after 1 year were 24% less than the preoperative scores (p < 0.01) and 55% less than after 1 week (p < 0.001). It was found that adenosine infusion induced a 57% increase in average defect score preoperatively (p < 0.001) but no increase postoperatively. No differences were seen between regions supplied by arterial or venous grafts. Isotope uptake defects increased between 1 h and 1 week after CABG surgery, and after 1 year the scores were less than those recorded preoperatively and after 1 week. Adenosine-induced reversible isotope uptake changes seen preoperatively were eliminated postoperatively in all vessel regions.

Adenosine↗
PubMed1998

The early critical phase of severe head injury: importance of apnea and dysfunctional respiration.

BACKGROUND: Apnea is a known response of concussive head injury. Hypoxic or ischemic brain injury has been documented in a high percentage of severe head injury deaths. The respiratory response after head injury remains poorly defined, however, and its contribution to hypoxic or ischemic mechanisms after severe head injury is unknown. METHODS: Eighteen anesthetized but spontaneously breathing rats were subjected to fluid percussion head injury of varying severities. Respiratory rate and volume of air were recorded before and after injury with a Hans Rudolph/Varadyne pneumotach differential pressure transducer and graphically measured. Postmortem inspection of the brains was performed. RESULTS: Apnea and subsequent respiratory dysfunction are directly proportional to the magnitude of energy delivered to the brain. Higher energy results in a dysfunctional or absent respiratory response, probably attributable to failure or disorganized function of the medullary respiratory center. CONCLUSION: This study for the first time graphically depicts the respiratory response after head injury. Higher energy delivered to the brain directly correlates with a markedly abnormal respiratory response that probably contributes significantly to subsequent hypoxic or ischemic brain injury. The absence of the space-occupying hematoma or gross parenchymal disruption suggests that in the clinical setting many of these patients may otherwise have survivable head injury if rescued by early ventilatory assistance.

Animals↗
PubMed1998

Adrenoleukodystrophy: unusual clinical and radiographic manifestation.

Adrenoleukodystrophy is an X-linked recessive peroxisomal disorder, characterized by progressive neurologic deterioration due to cerebral white matter demyelination and adrenal insufficiency. Onset is usually in childhood between ages 5 and 10, and its course is fatal within approximately 5 years. Initial symptoms are behavioral, gait, and auditory disturbances and may be a diagnostic dilemma. Abnormally raised plasma very long chain fatty acids (VLCFA) are diagnostic; computed tomography and magnetic resonance imaging findings show symmetrical occipital white matter lesions which progress in a rostralcaudal direction.

Adolescent↗
PubMed1998

Polyunsaturated fatty acids are lower in blood lipids of Usher's type I but not Usher's type II.

PURPOSE: Previous studies have shown that persons with retinitis pigmentosa and Usher's syndrome have lower blood levels of long-chain polyunsaturated fatty acids (PUFAs). In this study, the fatty acid composition of phospholipids from plasma and red blood cells (RBCs) was compared in persons with Usher's syndrome type I; Usher's syndrome type II; or no retinal disease (control subjects). METHODS: Blood was drawn from fasting volunteers and separated into plasma and RBCs by centrifugation. Lipids were extracted and phospholipids were obtained by thin-layer chromatography. Fatty acid methyl esters were prepared and analyzed by gas-liquid chromatography. RESULTS: There were no differences in plasma or RBC phospholipid fatty acid composition between control subjects (n = 54) and persons with Usher's syndrome type II (n = 20). However, all 20- and 22-carbon PUFA levels from RBCs of persons with Usher's syndrome type I were lower than those from control subjects and persons with Usher's Syndrome type II. Likewise, plasma levels of 20:3n-6, 20: 5n-3, and 22:6n-3 were lower in Usher's syndrome type I compared with the control group. In contrast, plasma levels of 18:1n-9 and RBC levels of 16:0 and 18:1n-9 were higher in the group with Usher's syndrome type I. CONCLUSIONS: Plasma and RBCs from Usher's syndrome type I, but not type II, have lower levels of long-chain PUFAs than plasma and RBCs from control subjects.

Adult↗
PubMed1997

Identification and quantitation of the fatty acids composing the CoA ester pool of bovine retina, heart, and liver.

Several proteins found in retinal photoreceptor cells (guanylate cyclase activating protein, protein kinase A, recoverin, and transducin) are N-terminally modified with the fatty acids 12:0, 14:0, 14:1n-9, and 14:2n-6, whereas similar proteins in other tissues contain only 14:0. It has been hypothesized that the acyl-CoA pool of the retina contains amounts of 12:0, 14:1n-9, and 14:2n-6 elevated over 14:0, in comparison to other tissues, and this accounts for the specificity of N-terminal fatty acylation. To test this hypothesis, we performed fatty acid analysis on total acyl-CoAs purified from bovine retina (light-adapted), heart, and liver. We also examined the N- and S-linked fatty acid composition of the total protein pools from these tissues. Acyl-CoAs were prepared from heart, liver, and retina and separated by high performance liquid chromatography (HPLC). Identities of peaks were based on HPLC of standard 12:0, 14:0, 14:1n-9, and 14:2n-6 CoAs. Total protein was subjected to base hydrolysis followed by acidic methanolysis to release S- and N-linked fatty acids, respectively, and fatty acid phenacyl esters were prepared for HPLC analysis. Retina had levels of 12:0 (2.7 +/- 2.1%), 14:1n-9 (2.9 +/- 2.2%), and 14:2n-6 (1.6 +/- 0.7%) CoAs below that of 14:0 CoA (7.0 +/- 1.8%). Likewise, heart levels of 14:2n-6 CoA (3.7 +/- 0.1%) were near and 12:0 (2.6 +/- 0. 6%) and 14:1n-9 (0.7 +/- 0.3%) CoAs were below that of 14:0 CoA (3.8 +/- 1.0%). Liver had levels of 12:0 (16.1 +/- 5.7%) and 14:2n-6 (8.1 +/- 1.2%) CoAs above and 14:1n-9 CoA (1.2 +/- 0.6%) below that of 14:0 CoA (5.9 +/- 0.8%). Fatty acid analysis of total protein showed that all tissues contained S-linked 16:0, 18:0, and 18:1n-9. Retina proteins contained N-linked 14:0, 14:1n-9, and 14:2n-6, whereas heart and liver had only 14:0. Our findings do not support the hypothesis that the CoA ester pool of the retina is enriched with 12:0, 14:1n-9, and 14:2n-6 over 14:0, in comparison to other tissues. This suggests that alternative models must be considered for the regulation of N-terminal fatty acylation of proteins in photoreceptor cells.

Acyl Coenzyme A↗
PubMed1997

Lipids of plasma, retina, and retinal pigment epithelium in Swedish briard dogs with a slowly progressive retinal dystrophy.

Reduced blood levels of long chain polyunsaturated fatty acids have been reported in humans and animals with inherited retinal degenerations. The lipid and fatty acid compositions of plasma, retina, and retinal pigment epithelium of the Swedish Briard dog, which has a very slowly progressive retinal dystrophy that is inherited in an autosomal recessive manner were analysed. The lipid class composition of the pigment epithelium was not different between affected and normal dogs; however, significant differences were found between the retinas of the two groups. Affected dogs had relatively more phosphatidylethanolamine and phosphatidylinositol and less phosphatidylcholine than normal dogs. There was no difference in the fatty acid compositions of plasma and retinal pigment epithelium between affected and normal dogs. However, the retinas of affected dogs had significantly lower levels of 22:5n-3 and 22:6n-3 and higher levels of 18:2n-6, 20:4n-6, and 22:5n-6. The total n-3 fatty acid content was significantly lower in affected retinas (P < 0.001), whereas the content of n-6 fatty acids was significantly higher in affected retinas (P < 0.001). These studies provide evidence for yet another animal model of inherited retinal degeneration with a defect in retinal polyunsaturated fatty acid metabolism. The fatty acid pattern in affected dogs resembles that seen in the retina in n-3 fatty acid deficiency.

Animals↗
PubMed1997

Effect of dietary linoleic/alpha-linolenic acid ratio on growth and visual function of term infants.

OBJECTIVES: To determine the effect of alpha-linolenic acid (ALA) intake (or the dietary linoleic acid [LA]/ALA ratio) on the growth and visual function of term infants. STUDY DESIGN: Normal term infants were assigned randomly and in masked fashion at birth to receive formulas with approximately 16% of total fatty acids as LA and 0.4%, 1.0%, 1.7%, or 3.2% of fatty acids as ALA (LA/ALA ratios of 44, 18.2, 9.7, and 4.8) for the first 4 months of life. The fatty acid pattern of plasma phospholipids was determined shortly after birth and at approximately 21, 60, and 120 days of age. Anthropometric data were obtained at the same times and also at approximately 240 days of age. Transient visual evoked responses (VERs) were measured at approximately 120 and 240 days of age. For comparisons, anthropometric and VER data also were obtained in infants who were exclusively breast-fed for the first 4 months of life. RESULTS: Infants who received the formula with 3.2% ALA (LA/ALA ratio, 4.8) had higher plasma concentrations of phospholipid docosahexaenoic acid (DHA) but lower concentrations of arachidonic acid at 21, 60, and 120 days of age. Mean weight of this group at 120 days of age was 760 gm less (p < 0.05) than the mean weight of the group that received the formula with 0.4% ALA (LA/ALA ratio, 44). Despite differences in plasma phospholipid DHA contents among groups, neither VER latency nor amplitude differed significantly among formula groups or between any formula group and age-matched, breast-fed infants. CONCLUSIONS: The highest versus the lowest ALA intake (or the lowest vs the highest LA/ALA ratio) resulted in higher plasma phospholipid DHA content from 21 to 120 days of age but was not associated with improved visual function as assessed by transient VER. Moreover, mean body weight of infants who received the highest versus lowest ALA intake was less at 120 days (p < 0.05). These data suggest that the lower LA/ALA ratios currently recommended for infant formulas should not be adopted until the effect of such ratios on growth are evaluated more completely.

Arachidonic Acids↗
PubMed1997

Hemodynamic response to adenosine infusion before and after coronary artery bypass surgery.

This study describes the hemodynamic dose-response characteristics of a titrated, continuous adenosine infusion before and 1 h (anesthetized), 1 week, and 1 year after coronary artery bypass graft (CABG) surgery. Average tolerated adenosine infusion rates were less 1 h and 1 week after surgery (128 +/- 23 and 118 +/- 27 microg/kg/min, respectively) than before (156 +/- 29 microg/kg/min) and 1 year after surgery (156 +/- 24 microg/kg/min). Heart rate (HR) increased with a 120-microg/kg/min adenosine infusion rate both preoperatively (21 +/- 11%) and 1 year postoperatively (16 +/- 8%). Systolic blood pressure (BP) decreased 26 +/- 11%, 14 +/- 7%, and 9 +/- 6% with 120 microg/kg/min adenosine for the three postoperative examinations. The integral of the outflow tract velocity with 120 microg/kg/min adenosine increased 49 +/- 22% and 29 +/- 12% after 1 h and 1 week, respectively, whereas its product with HR increased equally for all examinations (40 +/- 22%, 62 +/- 27%, 46 +/- 13%, and 39 +/- 11%). The average preoperative left ventricular area shortening was 45 +/- 10% and neither it nor end-diastolic left ventricular area (preload) changed with surgery, time after surgery, or with adenosine. A titrated adenosine infusion is well suited to patients requiring a pharmacologic provocation to expose reversible myocardial ischemia during the first hours or days after CABG surgery. The anesthetized and anemic patient are particularly unsuited for the commonly used fixed-infusion-rate protocol.

Adenosine↗
PubMed1997

Intermediates in endogenous synthesis of C22:6 omega 3 and C20:4 omega 6 by term and preterm infants.

An alternative pathway of omega 3 and omega 6 fatty acid metabolism has been described in isolated rate hepatocytes and human fibroblasts. This alternative pathway, which is independent of delta 4 desaturation, involves elongation of C22 5 omega 3 and C22:4 omega 6 to C24 fatty acids, delta 6 desaturation of the C24 fatty acids and subsequent beta oxidation of the desaturated products to C22:6 omega 3 and C22:5 omega 6. To determine whether this alternative pathway is operative in the human infant and also to obtain additional information concerning endogenous conversion of C18:3 omega 3 and C18:2 omega 6 to longer chain more unsaturated fatty acids, presence of [M + 18] isotopomers of omega 3 and omega 6 fatty acids in the plasma phospholipid fraction of term and preterm infants after administration of [U-13C]18:3 omega 3 and [U-13C]18:2 omega 6 was determined by negative chemical ionization gas chromatography/mass spectrometry. [M + 18] isotopomers of the following omega 3 fatty acids were detected: C18:3, C18:4, C20:3, C20:4, C20:5, C22:4, C22:5, C22:6, C24:4 (two infants only), C24:5, and C24:6. [M + 18] isotopomers of omega 6 fatty acids detected included only C18:2, C18:3, C20:2, C20:3, and C20:4, but sensitivity was insufficient to detect [M + 18] isotopomers of C22 and C24 omega 6 fatty acids. Presence of [M + 18] isotopomers of C24:5 omega 3 and C24:6 omega 3 indicates that these fatty acids were synthesized endogenously from C18:3 omega 3. This plus the in vitro data strongly suggests that infants use the recently described alternative pathway in endogenous synthesis of C22:6 omega 3. However, involvement also of delta 4 desaturation cannot be excluded. Detection of [M + 18] isotopomers of C20:3 omega 3, C20:2 omega 6, and C22:4 omega 3 suggests that C18:3 omega 3, C18:2 omega 6, and C20:4 omega 3 are elongated as well as desaturated. The specific fate of these elongation products and their importance in endogenous synthesis of omega 3 and omega 6 long chain polyunsaturated fatty acids remain to be determined.

Arachidonic Acid↗
PubMed1997

Polyunsaturated fatty acid metabolism in retinal and cerebral microvascular endothelial cells.

Docosahexaenoic acid (22:6n-3), an n-3 essential fatty acid derived from elongation and desaturation of linolenic acid (18:3n-3), is found in abundant proportion in the brain and the retina. It is generally assumed that the liver is the major source of 22:6n-3 for these organs, although some retinal and cerebral cells, such as retinal pigment epithelium (Wang and Anderson, 1993. Biochemistry. 32:13703-13709) and brain astrocytes (Moore et al. 1991. J. Neurochem. 56:518-524) have the ability to produce 22:6n-3. The aim of the present study was to determine whether retinal and cerebral microvascular endothelium could synthesize 22:6n-3. After incubation of both cultured bovine retinal and rat cerebral endothelial cells with [3-14C] 22:5n-3 in presence of serum, radioactivity was primarily recovered in 20:5n-3, indicating active retroconversion reactions in both tissues. However, 22:6n-3, 24:5n-3, and 24:6n-3 were also labeled. All of these metabolites were released in the medium as free fatty acids. Retinal endothelial cells preferentially released labeled 24-carbon metabolites, whereas cerebral endothelial cells released relatively more 20:5n-3 and 22:6n-3. With heat-inactivated serum or no serum, both endothelial cell preparations showed relatively higher retroconversion levels. However, in serum-deprived cells, the elongation/desaturation pattern was affected in retinal cells only, with an accumulation of 24:5n-3 relative to a decrease of 24:6n-3 and 22:6n-3. Fatty acid composition analyses revealed a decrease in long-chain polyunsaturated n-6 and n-3 fatty acids in retinal cells maintained in inactivated serum compared to normal serum, while no change was found in cerebral cells. Taken together, these results suggest that 1) the synthesis of 22:6n-3 by both retinal and cerebral endothelial cells is independent of a delta4-desaturase; 2) retinal and cerebral endothelia could be a source of 22:6n-3 for the retina and the brain, respectively; and 3) retinal endothelial delta6-desaturase, which converts 24:5n-3 to 24:6n-3, could be stimulated by serum components.

Animals↗
PubMed1997

Phosphatidylinositol 3-kinase in bovine photoreceptor rod outer segments.

PURPOSE: Phosphatidylinositol 3-kinase (PI 3-kinase) plays important roles in mitogenesis, vesicular trafficking, actin rearrangement, and prevention of apoptotic cell death in nonocular tissues. This investigation looked for whether PI 3-kinase is present in bovine rod photoreceptors and if light has any effect on its activity. METHODS: Bleached (BROS) and dark-adapted (DROS) rod outer segments were prepared from frozen bovine retinas and immunoblotted or immunoprecipitated with antibodies against the regulatory (p85) or catalytic (p110) subunits of PI 3-kinase. Kinase activity was measured in the immunoprecipitates and the reaction products were identified by high-performance liquid chromatography (HPLC). The amount of PI 3-kinase in membrane and cytosol fractions was determined by densitometry of immunoblots. RESULTS: Immunoblot analysis showed the presence of 85 and 110 kDa proteins in ROS. PI 3-kinase immunoprecipitated by anti-p85 antibody converted PI to PI-3-P and PI-4-P to PI-3,4-P2, as determined by HPLC analysis of the deacylated products. The PI 3-kinase activity in these ROS preparations was sensitive to wortmannin, a potent inhibitor of PI 3-kinase, at low concentrations (IC50 3 nM). Immunoprecipitates (IPs) showed activity twice as high in BROS as in DROS. The IPs of ROS membranes but not cytosol maintained the light-dark difference. However, measurement of anti-p85 and anti-p110 immunoreactivities on western blots of ROS, ROS membranes, and ROS cytosol did not show any light-dark differences. CONCLUSIONS: PI 3-kinase is present in bovine rod outer segments and its activity appears to be greater in light-adapted retinas.

Animals↗
PubMed1997

Light exposure induces ubiquitin conjugation and degradation activities in the rat retina.

PURPOSE: To evaluate the consequences of light exposure on retinal ubiquitin (Ub) conjugation and degradation. METHODS: Two-month-old Long Evans pigmented rats were exposed to constant light (180 foot-candles) or were left in complete darkness for 18 hours. Rats used for cyclic light and diurnal rhythm experiments were removed from their light cycles at different times (24-hour clock): 0700 (before the light was turned on), 1000 (3 hours into the light cycle), 1000D (continued in the dark cycle), 1900 (before the light was turned off), 2200 (3 hours into the dark cycle), and 2200L (continued in the light cycle). The retinas were examined for Ub conjugation, adenosine triphosphate-Ub-dependent degradation, levels of Ub messenger RNA, and localization of Ub immunocytochemistry. RESULTS: There was a statistically significant increase in Ub conjugation and degradation in retinas isolated from light-exposed animals compared with degradation in retinas of dark-adapted animals. However, no significant differences were observed in the levels of Ub messenger RNA from cyclic light, or light-exposed or dark-adapted retinas, suggesting that light-stress-induced changes do not reflect increased transcriptional activity. The daily variations observed in Ub conjugation and degradation suggest that these processes are probably the result of a circadian rhythm. Results of immunohistochemical studies revealed that Ub and its conjugates were uniformly distributed throughout the retinal cell layers in light- and dark-adapted retinas. However, in light-exposed retinas, a strong positive immunoreactivity was observed in the inner retina, specifically in horizontal and ganglion cells. CONCLUSIONS: These results suggest that light exposure may play a role in inducing Ub-conjugating activity in certain retinal cells. Furthermore, the results support the hypothesis that Ub is a stress protein that plays an important role in protecting cells under stress conditions.

Adenosine Triphosphate↗
PubMed1997

Diets enriched in docosahexaenoic acid fail to correct progressive rod-cone degeneration (prcd) phenotype.

PURPOSE: Results of a previous study show abnormal plasma lipids in progressive rod-cone degeneration (prcd)-affected dogs, with lower docosahexaenoic acid (DHA; 22:6n-3) and cholesterol levels but no differences in other plasma fatty acids, lipids, triglycerides, and fat-soluble vitamins. There is also an increase of the DHA precursor 22:5n-3, so that the ratio of 22:5n-3 to 22:6n-3 is higher in affected than in normal dogs. Because DHA is the predominant esterified fatty acid in rod outer segment (ROS) phospholipids, these findings suggest a possible causal association between abnormal plasma lipid levels and retinal degeneration. In the current study, dietary supplements rich in 22:6n-3 were used to determine whether plasma, liver, and rod outer segment phospholipid composition can be altered to modify the prcd disease phenotype. METHODS: prcd-affected and normal control dogs were given DHA-enriched supplements for short (7- and 25-day) and long (21-week) periods, and the fatty acid composition of plasma, liver, and rod outer segment phospholipids were examined. In the long-term study, electroretinography and morphology were used to assess modification of the retinal degeneration phenotype. RESULTS: Administration of DHA-enriched supplements resulted in increases in plasma DHA and n-3 polyunsaturated fatty acids and in decreases in some n-6 fatty acids in normal and prcd-affected dogs. Similar increases in DHA and n-3 fatty acids were observed in the liver, but affected dogs had significantly higher levels at all supplementation time points examined. In contrast, the ROS of affected dogs had statistically lower (approximately 20%) DHA levels, and these levels could not be increased with dietary supplementation. The disease phenotype could not be modified by DHA-enriched supplements. CONCLUSIONS: Regardless of the sustained three- to fourfold elevation in plasma and liver DHA that occurs as the result of supplementation, the ROS DHA levels remain unchanged, and the prcd disease phenotype is not modified by the dietary manipulation. These findings could be the result of a reduction in the synthesis of DHA-containing phospholipids in the retinas of affected dogs; or, alternatively, there could be a reduction in DHA uptake, transport, or storage within the retinal pigment epithelium-photoreceptor complex.

Animals↗