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Background Arachidonic acid (AA, C20:4, ω-6) is a ω-6 polyunsaturated fatty acid (PUFA) and plays diverse roles in cell signaling. Numerous reports on the effects of ω-3 PUFAs, such as docosahexaenoic acid (DHA, C22:6, ω-3) and eicosapentaenoic acid (EPA, C20:5, ω-3) on learning and memory impairments of rats are available, however, the role of AA on brain cognition is largely unknown. Objective In this study, our aim was to investigate the effect of oral administration of AA on spatial memory-related learning ability in aged (100 weeks) male rats. Design One group was per orally administered 240 mg/kg per day AA oil and the other group was administered the similar volume of control oil. Five weeks after the start of the administration, rats were tested with the partially baited eight-arm radial maze to evaluate two types of spatial memory-related learning ability displayed by reference memory errors (RMEs) and working memory errors (WMEs). Also, the time required to complete the task was recorded. The levels of lipid peroxide (LPO) and reactive oxygen species (ROS) were measured, as an indicator oxidative stress in the plasma and brain corticohippocampal brain tissues. Results The scores of RMEs and WMEs, which are analogous to long-term and short-term memory, respectively, were not affected, however, the trial time was shorter in the AA-administered rats than that of the controls. AA also significantly increased the degree of oxidative stress both in the plasma and corticohippocampal brain tissues. Conclusions Our results suggest that though AA deposition in the corticohippocampal tissues of senescent rats caused a faster performance activity, which is reminiscent to hyperactive behavior of animals, the spatial learning ability-related memory of the rats, however, was not improved.

Background: The herb, Commelina paludosa (CP) Blume (Family-Commelinaceae) is medicinally used by the traditional practitioners in Bangladesh. However, there is a lack of scientific evidence on this medicinal herb. Aim and Objectives: This study aimed to evaluate the phytochemical and pharmacological activities of CP (ethanol [ECP], chloroform [CCP] and n-hexane [NHCP] of whole-plant extracts). Materials and Methods: For this antioxidant, antimicrobial, antidiarrheal and antipyretic activities of crude extracts of CP were conducted by 1,1-diphenyl-2-picrylhydrazyl (DPPH) scavenging, disc diffusion and serial dilution, castor oil-induced diarrhea and yeast powder-induced pyrexia methods respectively. Results and Observation: The results suggest that all the fractions significantly scavenged DPPH radicals. In the disc diffusion test, the zones of inhibition were observed within the range of 7 mm to 30.67 mm at 500 mg/disc. The highest zones of inhibition were observed by ECP, CCP and NHCP against Bacillus azotoformans, Lactobacillus coryifomis and Salmonella typhi respectively. NHCP was found to exert stronger antibacterial effect than the ECP and CCP. Conclusion: Minimum inhibitory concentrations were detected within the range of 31.25 and 250 μg/ml. Moreover, the crude fractions also showed significant (P < 0.05) antidiarrheal and antipyretic activities in Swiss mice. CP may be a good source of therapeutic components.

The presence of lead (Pb) in fetal brain may affect brain development-related proteins. We studied whether gestational/lactational Pb-exposure affects oxidative stress, proinflammatory response, apoptosis and levels of brain development/cognition-related proteins, including presynaptic synaptosome-associated protein-25 (SNAP-25), postsynaptic density protein-95 (PSD-95), brain-derived neurotropic factor (BDNF), tyrosine receptor-kinase protein B (TrkB) and vesicular acetylcholine transporter (VAChT) in the offspring. Female Wistar rats were randomly divided into control and Pb-exposed mother groups. The Pb-exposed rats received 0.1% (w/v) Pb acetate via drinking water during pregnancy and lactation. Milk and mammary glands were collected from lactating mothers to measure milk/mammary gland levels of lipid peroxide (LPO), as indicator of oxidative stress and proinflammatory TNF-α. Afterwards, the pups were sacrificed to determine brain levels of Pb, LPO, TNF-α, cytochrome C, SNAP-25, PSD-95, BDNF, TrkB and VAChT. The levels of LPO and TNF-α increased in the milk/mammary glands of the Pb-exposed mothers, concurrently with increases in the levels of Pb, LPO, TNF-α and cytochrome C and decreases in the levels of SNAP-25, PSD-95, BDNF, TrkB and VAChT in the brains of their offspring. Our results demonstrate that Pb-exposure during development reduces the brain levels of PSD-95 and SNAP-25 (synaptogenesis-markers), with concomitant upsurges of oxidative stress, TNF-α and apoptosis in the offspring. Furthermore, BDNF-TrkB proteins that comprehend memory-related brain cognitions and/or VAChT that comprises cholinergic-neuromotor activities might be impaired by Pb-exposure. These findings provide evidence of toxic effects of Pb on brain development, at least, partially by decreasing the levels of PSD-95, SNAP-25 and other cognition-related proteins.

The accumulation of amyloid β peptide1-42 (Aβ1-42) masses in the brains of Alzheimer’s Disease (AD) patients is associated with neuronal loss and memory deficits. We have previously reported that oral administration of docosahexaenoic acid (DHA, C22:6, n-3) significantly decreases Aβ burden in the brains of AD model rats and that direct in vitro incubation of DHA with Aβ1-42 curbs the progression of amyloid fibrillation. In the present in silico study, we investigated whether DHA computationally binds with amyloid peptides. The NMR solution structures of Aβ1-42 were downloaded from the Protein Data Bank (PDB IDs: 1Z0Q and 2BEG). The binding of DHA to Aβ peptides was assessed by molecular docking using both a flexible and rigid docking system. Thioflavin T (ThT) was used as positive control. The chemical structures of ThT and DHA were modeled and converted to the PDB format using PRODRUG. Drug-like properties of DHA were evaluated by ADME (Absorption, Distribution, Metabolism, and Excretion). DHA was found to successfully dock with Aβ1-42. Computational analyses of the binding of DHA to Aβ1-42, as evaluated by docking studies, further corroborated the inhibitory effect of DHA on in vitro Aβ1-42 fibrillogenesis and might explain the in vivo reduction of amyloid burden observed in the brains of DHA-administered AD model rats demonstrated in our previous study. These computational data suggest the potential utility of DHA as a preventive medication in Aβ-induced neurodegenerative diseases, including AD.

Aim We examined the effects of the administration of docosahexaenoic acid (DHA)-enriched meals on cognitive function in the oldest elderly with cognitive impairment, such as dementia, living in nursing homes, and on the improvement in caregiver burden at aging agencies. Methods Participants in elderly care facilities and nursing homes (n = 75; 88.5 ± 0.6 years) were randomized in active and placebo groups. The active group had family-style meals containing an additional 1720 mg of docosahexaenoic acid per day for 12 months. At baseline, and after 6 and 12 months of intervention, cognitive function was assessed using Hasegawa's Dementia Scale-Revised and the Mini-Mental State Examination; mental health condition was assessed with the Apathy scale and the Zung Self-Rating Depression Scale; caregiver burden was evaluated using Zarit Burden Interview scores; and participants’ serum biochemical factors were measured. Results The participants were suggested to have dementia. After 12 months, the mean change in Mini-Mental State Examination subitem “Registration” score from baseline to month 12 showed a tendency to be greater in the active group than that in the placebo group. Mean changes in the Apathy scale from baseline to month 12 were less, and the changes in the Zung Self-Rating Depression Scale and the total Zarit Burden Interview scores showed a tendency to be lower in the active group than in the placebo group, respectively. Conclusion These results suggest that docosahexaenoic acid-enriched meals protect against age-related cognitive decline, and also improve apathy and caregiver burden for the oldest-elderly Japanese with cognitive impairment, such as dementia. Geriatr Gerontol Int 2017; 17: 330–337.

The accumulation of amyloid β peptide1-42 (Aβ1-42) masses in the brains of Alzheimer’s Disease (AD) patients is associated with neuronal loss and memory deficits. We have previously reported that oral administration of docosahexaenoic acid (DHA, C22:6, n-3) significantly decreases Aβ burden in the brains of AD model rats and that direct in vitro incubation of DHA with Aβ1-42 curbs the progression of amyloid fibrillation. In the present in silico study, we investigated whether DHA computationally binds with amyloid peptides. The NMR solution structures of Aβ1-42 were downloaded from the Protein Data Bank (PDB IDs: 1Z0Q and 2BEG). The binding of DHA to Aβ peptides was assessed by molecular docking using both a flexible and rigid docking system. Thioflavin T (ThT) was used as positive control. The chemical structures of ThT and DHA were modeled and converted to the PDB format using PRODRUG. Drug-like properties of DHA were evaluated by ADME (Absorption, Distribution, Metabolism, and Excretion). DHA was found to successfully dock with Aβ1-42. Computational analyses of the binding of DHA to Aβ1-42, as evaluated by docking studies, further corroborated the inhibitory effect of DHA on in vitro Aβ1-42 fibrillogenesis and might explain the in vivo reduction of amyloid burden observed in the brains of DHA-administered AD model rats demonstrated in our previous study. These computational data suggest the potential utility of DHA as a preventive medication in Aβ-induced neurodegenerative diseases, including AD.

Summary Congenital adrenal hyperplasia (CAH) due to the three-beta-hydroxysteroid-dehydrogenase (3β-HSD) enzyme deficiency is a rare autosomal recessive disorder presenting with sexual precocity in a phenotypic male. Klinefelter syndrome (KS) is the most common sex chromosome aneuploidy presenting with hypergonadotropic hypogonadism in a male. However, only a handful of cases of mosaic KS have been described in the literature. The co-existence of mosaic KS with CAH due to 3β-HSD enzyme deficiency portrays a unique diagnostic paradox where features of gonadal androgen deficiency are masked by simultaneous adrenal androgen excess. Here, we report a 7-year-old phenotypic male boy who, at birth presented with ambiguous genitalia, probably a microphallus with penoscrotal hypospadias. Later on, he developed accelerated growth with advanced bone age, premature pubarche, phallic enlargement and hyperpigmentation. Biochemically, the patient was proven to have CAH due to 3β-HSD deficiency. However, the co-existence of bilateral cryptorchidism made us to consider the possibility of hypogonadism as well, and it was further explained by concurrent existence of mosaic KS (47,XXY/46,XX). He was started on glucocorticoid and mineralocorticoid replacement and underwent right-sided orchidopexy on a later date. He showed significant clinical and biochemical improvement on subsequent follow-up. However, the declining value of serum testosterone was accompanied by rising level of FSH thereby unmasking hypergonadotropic hypogonadism due to mosaic KS. In future, we are planning to place him on androgen replacement as well. Learning points: Ambiguous genitalia with subsequent development of sexual precocity in a phenotypic male points towards some unusual varieties of CAH. High level of serum testosterone, adrenal androgen, plasma ACTH and low basal cortisol are proof of CAH, whereas elevated level of 17-OH pregnenolone is biochemical marker of 3β-HSD enzyme deficiency. Final diagnosis can be obtained with sequencing of HSD3B2 gene showing various mutations. Presence of bilateral cryptorchidism in such a patient may be due to underlying hypogonadism. Karyotyping in such patient may rarely show mosaic KS (47,XXY/46,XX) and there might be unmasking of hypergonadotropic hypogonadism resulting from adrenal androgen suppression from glucocorticoid treatment.

Memory extinction is referred to as a learning process in which a conditioned response (CR) progressively reduces over time as an animal learns to uncouple a response from a stimulus. Extinction occurs when the rat is placed into a context without shock after training. Docosahexaenoic acid (DHA, C22:6, n-3) is implicated in memory formation in mammalian brains. In a two-way active shuttle-avoidance apparatus, we examined whether DHA affects the extinction memory and the expression of brain cognition-related proteins, including gastrin-releasing peptide receptor (GRPR), brain-derived neurotrophic factor receptor (BDNFR) tyrosine kinase receptor B (TrKB), and N-methyl-d-aspartate receptor (NMDAR) subunits NR2A and NR2B. Also, the protein levels of GRP, BDNF, postsynaptic density protein-95 (PSD-95), and vesicular acetylcholine transporter (VAChT), and the antioxidative potentials, in terms of lipid peroxide (LPO) and reactive oxygen species (ROS), were examined in the hippocampus. During the acquisition phase, the rats received a conditioned stimulus (CS-tone) paired with an unconditioned stimulus (UCS foot shock) for three consecutive days (Sessions S1, S2, and S3, each consisting of 30-trials) after 12 weeks of oral administration of DHA. After a three-day interval, the rats were re-subjected to two extinction sessions (S4, S5), each comprising 30 trials of CS alone. During the acquisition training in S1, the shock-related avoidance frequency (acquisition memory) was significantly higher in the DHA-administered rats compared with the control rats. The avoidance frequency, however, decreased with successive acquisition trainings in sessions S2 and S3. When the rats were subjected to the extinction sessions after a break for consolidation, the conditioned response (CR) was also significantly higher in the DHA-administered rats. Interestingly, the freezing responses (frequency and time) also significantly decreased in the DHA-administered rats, thus suggesting that a higher coping capacity was present during fear stress in the DHA-administered rats. DHA treatments increased the mRNA levels of GRPR, BDNF receptor TrKB, and NMDAR subunit NR2B. DHA also increased the protein levels of GRP, BDNF, PSD-95, and VAChT, and the antioxidative potentials in the hippocampus. These results suggest the usefulness of DHA for treating stress disorders.

We studied on the effect of Curcuma longa extract on spatial learning-related memory ability of old rats in eight-arm radial maze task. Rats were randomly divided into two groups: one group was orally administered 100 mg/KgBW/day C. longa extract (CLE) dissolved in deionized water and the other group was administered the vehicle alone for 10 weeks. The rats were tested with the partially baited eight-arm radial maze to evaluate two types of spatial memory-related learning ability displayed by reference memory errors (RMEs) and working memory errors (WMEs). Chronic administration of CLE significantly decreased the number of RMEs and WMEs, concurrently with the decreases in the cortico-hippocampal levels of lipid peroxides (LPO) and tumor necrosis factor alpha (TNF-α). In a parallel set of experiments, CLE-pretreated rats of the same age group were subjected to hypoxia-reperfusion injury by carotid artery occlusion to induce oxidative stress in the brains in order to examine whether such an in vivo hypoxia-induced oxidative stress could be ameliorated by the extract. Again, the levels of LPO were significantly decreased in the cortico-hippocampal tissues of the CLE-fed hypoxic rats. The histology of the brains also revealed that the CLE-pretreated rats had retained improved cellular integrity. Finally, our results provide the evidence that oral administration of C. longa extract increases the defense against oxidative stress and proinflammatory TNF-α, concurrently with the improvement of memory-related brain cognitive ability of the aged rats.

The accumulation of amyloid β peptide 1 - 42 (Aβ1-42) in the brain of Alzheimer’s disease (AD) patients is known to be associated with neurodegeneration and memory impairment. More recently, we reported that madecassoside, an active component of Centella asiatica, improved memory impairment in an Aβ1-42 infusion rat model of AD, ameliorated neurotoxicity in SH-SY5Y cells, and inhibited in vitro Aβ1-42 fibril formation. In the present study, we investigated the utility of in silico analyses in corroborating observed in vivo and in vitro effects of madecassoside in AD to further assess the therapeutic benefits of madecassoside. The 3D structure of Aβ1-42 was downloaded from the Research Collaboratory for Structural Bioinformatics (RCSB) Protein Data Bank (PDB). The binding of madecassoside to Aβ1-42 was assessed by molecular docking. The chemical structure of madecassoside was modeled and converted to the PDB format. Madecassoside was found to successfully dock with Aβ1-42. Computational demonstration of the binding of madecassoside to Aβ1-42 further corroborated the inhibitory effect of madecassoside on Aβ1-42 fibrillogenesis which was demonstrated in our previous study. These data showed the potential utility of madecassoside as a preventive medication in Aβ1-42-induced neurodegenerative diseases such as AD.

Metabolic syndrome is implicated in the decline of cognitive ability. We investigated whether the prescription n-3 fatty acid administration improves cognitive learning ability in SHR.Cg-Lepr(cp)/NDmcr (SHR-cp) rats, a metabolic syndrome model, in comparison with administration of eicosapentaenoic acid (EPA, C20:5, n-3) alone. Administration of TAK-085 [highly purified and concentrated n-3 fatty acid formulation containing EPA ethyl ester and docosahexaenoic acid (DHA, C22:6, n-3) ethyl ester] at 300 mg/kg body weight per day for 13 weeks reduced the number of reference memory-related errors in SHR-cp rats, but EPA alone had no effect, suggesting that long-term TAK-085 administration improves cognitive learning ability in a rat model of metabolic syndrome. However, the working memory-related errors were not affected in either of the rat groups. TAK-085 and EPA administration increased plasma EPA and DHA levels of SHR-cp rats, associating with an increase in EPA and DHA in the cerebral cortex. The TAK-085 administration decreased the lipid peroxide levels and reactive oxygen species in the cerebral cortex and hippocampus of SHR-cp rats, suggesting that TAK-085 increases antioxidative defenses. Its administration also increased the brain-derived neurotrophic factor levels in the cortical and hippocampal tissues of TAK-085-administered rats. The present study suggests that long-term TAK-085 administration is a possible therapeutic strategy for protecting against metabolic syndrome-induced learning decline.

The aim of the study was to evaluate the effect of Leucas zeylanica against oxidative stress on hepatic tissue. Oxidative stress was induced by exposing hepatic tissue to ethanol and Fenton’s reagent (H2O2+FeSO4). The effect of oxidative stress on liver also was evaluated by the determination of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) activity and the levels of lipid peroxide (LPO). The antioxidative activity of L. zeylanica was determined by estimating it ability to inhibit the hepatic levels of lipid peroxide (LPO), as indicator of oxidative stress. Concomitantly, the antioxidant phytochemicals such as polyphenols and flavonoids were assessed against pyrogallol and quercetin standards. The ALT and AST activities and the levels of LPO of hepatic tissue were significantly increased by oxidative stress. L. zeylanica pretreatment, however, significantly repressed the oxidative stress on hepatic tissue, as indicated by the decreased activities of ALT and AST enzymes and levels of LPO. Analyses of the phytochemicals revealed that the extract of L. zeylanica contained substantial amounts of polyphenols (74.32 ± 4.6 µg of pyrogallol equivalent/mg) and flavonoids (15.69 ± 2.2 µg quercetin equivalent/mg of extract). Finally, the results of the present study demonstrated the presence of antioxidant phytochemicals, including polyphenols and flavonoids in L. zeylanica and henceforth conferred protection against ethanol and H2O2-induced oxidative stress on hepatic tissue.DOI: http://dx.doi.org/10.3329/icpj.v2i9.16076 International Current Pharmaceutical Journal, August 2013, 2(9): 148-151

To evaluate the effect of Ramadan fast on serum lipid profile status of men, the study was carried out in the National Mushroom Development and Extension Centre, Sobhanbag, Savar Dhaka in association with the Department of Pharmacy and Department of Biochemistry and Molecular Biology, Jahangirnagar University, Savar, Dhaka. The experiment was conducted before and after the Arabic month, Ramadan, when there occurs a change both in the pattern and timing of dietary intake. Findings of the study shows Ramadan fast significantly reduced serum Low Density Lipoprotein (LDL-C) (p = 0.011). A statistically non significant reduction of total Cholesterol (TC) (p = 0.340), small elevation of High Density Lipoprotein (HDL-C) (p = 0.252) and Triglyceride (TG) (p = 0.502) were also observed. Considering the findings of the study it was noticeable that one month Ramadan fast can improve lipid profile status of blood and hence able to improve atherosclerotic diseases which includes hypertension, ischemic heart disease and stroke. DOI: http://dx.doi.org/10.3329/jdnmch.v18i2.16021 J. Dhaka National Med. Coll. Hos. 2012; 18 (02): 37-42

Amyloid β(Aβ)1-42 fibrillation is a crucial step in the development of pathological hallmarks, such as neuritic plaques and neurofibrillary tangles, of Alzheimer’s disease (AD). In this study, we evaluated the effects of free docosahexaenoic acid (DHA), an essential brain polyunsaturated fatty acid (PUFA), on the inhibition of Aβ1-42 fibrillation by fluorescence correlation spectroscopy (FCS), a technique capable of detecting molecular movements and interactions in solution. We also examined whether free arachidonic acid (AA), eicosapentaenoic acid (EPA), and metabolites of DHA, including neuroprotectin D1 (NPD1, 10S, 17S-dihydroxy-DHA), resolvin D1 (RvD1, 7S, 8R, 17S-trihydroxy-DHA), and didocosahexaenoyl glycerol (diDHA), affect Aβ1-42 polymerization. The results of the FCS study reveal that DHA and AA significantly reduced the diffusion time of TAMRA (5-carboxytetramethylrhoda-mine)-Aβ1-42 by 28% and 31%, respectively, while EPA, NPD1, RvD1, and diDHA had no effects on diffusion time. These results indicate that DHA and AA inhibited Aβ1-42 polymerization and that their inhibitory effects occurred at the initial stage of Aβ1-42 polymerization. This study will advance the research on PUFAs in preventing AD progression.

In this study, superfluous jute plants and jute stick were converted into upgraded animal feed by solid state fermentation (SSF) using a cellulolytic fungus, Pleurotus sajor-caju. Prior to fermentation, substrates were subjected to several pretreatments such as soaking with water overnight and alkali or lime pretreatment. SSF was carried out with 20 g of substrate in 100 ml conical flask and was incubated at 30C for 8 weeks. In all treatments, the highest amount of reducing sugar, soluble protein as well as the cellulolytic activities of three enzymes viz. cellobiase, carboxymethyl cellulase and avicelase were obtained at 6th week of fermentation. Compared to raw, unsoaked substrates, soaking treatment alone could produce 10% more soluble protein in both substrates whereas reducing sugar increment was 5% and 6% in jute sticks and jute plants, respectively. From all treatments, combination of soaking and lime treatment in green jute plants yielded higher value than jute sticks in terms of reducing sugar, soluble protein and enzymatic activity. The radiation doses at 20, 30 and 40 kGy appeared to have no effect on sugar and protein accretion. During eight weeks of fermentation, relatively higher cellobiase activity was found compared to that of carboxymethyl cellulase and avicelase. The present investigation indicates that fungal conversion with pretreatment can turn these lignocellulosic agro-wastes to a nutritionally enriched animal feed by increasing the crude protein and reducing sugar content. However, further research is necessary to develop strategies for industrial scale production to overcome the crisis of nutritionally improved animal feed.

Functional food can be either natural or processed. Food contains known biologically active compounds, which provides clinically proven and documented health benefit. So far, no database is available in Bangladesh regarding the functionality of the indigenous foods. As a primary step, this study had been conducted with an aim to identify and characterize functionality of the indigenous foods of Bangladesh. Eight fruits and vegetables, which are very popular for their taste, price and easy availability, have been selected for in vitro screening of their functionality. High levels of fat and sugar binding capacity were observed in Pineapple (500% and 270.891% respectively). High nuplli mortality rate was found in cytotoxicity test with Pomelo extract (100%), which also contained high level of vitamin C (155 mg/100g). Pomelo contained the highest level of antioxidant among all these foods (0.674 nMol/100μl/mg protein). Red amaranth contained highest amount of protein (4.31 g/100g). In stem amaranth, Iron level was highest (1855.67 mg/kg). Total phenolics content of Water spinach and Stem amaranth were found higher than the other samples (59.339 and 55.728 mg GAE/g respectively). All these experiments showed these vegetables and fruits have high health impacts and can be act as potential functional foods.

The high mortality rate in Bangladesh is related to poverty, which results in protein malnutrition, essential fatty acid deficiency and lacks in adequate vitamins, minerals and calorie. Exploring new food items with improved dietary nutrition factors may, therefore, help to decrease the mortality rate in the poor countries like Bangladesh. Accordingly, the present study was a proximate composition and fatty acid analysis of L. purpureus seed—a legume seed which is given no careful attention locally, though it might be a good source of valuable nutrition factors for both animals and humans. The purpose of the study was, therefore, to generate awareness that L. purpureus could also act as a good source of food components essential for good health. Proximate analysis revealed that the seed powder contained 8.47 ± 0.52% moisture; 3.50 ± 0.0.07% ash; 1.02 ± 0.06% total fat; 23.95 ± 0.15% total protein; 1.21 ± 0.16% total dietary fiber; 61.86 ± 0.70% total carbohydrate and 352.4 ± 2.66 kcal/100 g energy. Phytic acid content (%) was 1.014 ± 0.048. Major fatty acid composition (%): the essential fatty acid linoleic acid (C18:2, ω-6) was 9.50 ± 0.68, while the linolenic acid (C18:3, ω-3) was 1.95 ± 0.18. Palmitic acid (C16:0), stearic acid (C18:0) and oleic acid (C18:1) were, respectively, 2.96 ± 0.19, 0.77 ± 0.04 and 1.10 ± 0.06. Lignoceric acid (C24:0) was 0.11 ± 0.007%. Monounsaturated palmitoleic acid (0.006 ± 0.0), docosapentaenoic acid (DPA, C22:5, ω-3) and nervonic acid (0.002 ± 0.0) were present in trace amounts. Arachidonic acid (AA, C20:4, ω-6), eicosapentaenoic acid (C20:5, ω-3), and docosahexaenoic acid (C22:6, ω-3) were not detected. The fatty acid profile, thus, suggests that essential omega-6 fatty acid linoleic acid (C18:3, ω-6) and omega-3 linolenic acid (C18:3, ω-3) were the major polyunsaturated fatty acids (PUFA) present in L. purpureus seed. In addition, the seed contained high amount of proteins. Finally, these results suggest that L. purpureus seed could be used as a good source of quality food components, including protein and essential fatty acids.

Docosahexaenoic acid (DHA, C22:6, ω-3) is a highly polyunsaturated omega-3 fatty acid. It is concentrated in neuronal brain membranes, for which reason it is also referred to as a "brain food". DHA is essential for brain development and function. It plays an important role in improving antioxidant and cognitive activities of the brain. DHA deficiency occurs during aging and dementia, impairs memory and learning, and promotes age-related neurodegenerative diseases, including Alzheimer's disease (AD). For about two decades, we have reported that oral administration of DHA increases spatial memory acquisition, stimulates neurogenesis, and protects against and reverses memory impairment in amyloid β peptide-infused AD rat models by decreasing amyloidogenesis and protects against age-related cognitive decline in the elderly. These results demonstrate a robust link between DHA and cognitive health. Rodents that were fed a diet low in ω-3 polyunsaturated fatty acids, particularly those that were DHA-deficient, frequently suffered from anxiety, depression and memory impairment. Although the exact mechanisms of action of DHA in brain functions are still elusive, a host of mechanisms have been proposed. For example, DHA, which inherently has a characteristic three-dimensional structure, increases membrane fluidity, strengthens antioxidant activity and enhances the expression of several proteins that act as substrates for improving memory functions. It reduces the brain amyloid burden and inhibits in vitro fibrillation and amyloid-induced neurotoxicity in cell-culture model. In this review, we discuss how DHA acts as a molecule with diverse functions.

Myosin heavy chain (MHC) mediates the metabolic and contractile responses of skeletal muscles. MHC displays different isoforms, each of which has different characteristics. To better understand the effect of polyunsaturated fatty acids in skeletal muscles, rats were fed with control-, docosahexaenoic acid (DHA)-, and arachidonic acid (ARA)-oil, and the effects on plasma and muscular fatty acid profile, oxidative stress, mRNA levels of myosin heavy chain isoforms MHC1 of slow-twitch muscle (SO) and MHC2A, MHC2X, and MHCB isoforms of extensor digitorum longus (EDL) of fast-twitch muscle were evaluated. Concomitantly, mRNA levels of anti-oxidative enzymes, such as, catalase, glutathione peroxidase (GPx) and superoxide dismutase (SOD were determined. The expressions of MHC1, MHC2A, MHC2X, and MHC2B were lower in the SO of the DHA-fed rats. In the EDL muscles of DHA-fed rats, the expressions of MHC1 and MHC2A increased; however, the expressions of MHC2X increased and that of the MHC2 were not altered. Oxidative stress, as indicated by the levels of LPO, was significantly higher in the plasma of the ARA-fed rats, when compared with that of the DHA-fed rats. The LPO levels were higher both in the SO and EDL muscles of ARA-fed rats. Compared with ARA oil intake, DHA oil showed higher mRNA levels of GPx and SOD. Catalase expression was higher only in the EDL but not in the SO-type muscles. Our studies finally indicate that DHA and ARA differentially affect the regulation of contractile and metabolic properties of slow- and fast-twitch skeletal muscles.

Identifying dietary alternatives for artificial antioxidants capable of boosting antihemolytic and antioxidative defense has been an important endeavor in improving human health. In the present study, we studied antihemolytic and antioxidative effects of germosprout (i.e., the germ part along with sprouted stems plus roots) extract prepared from the pregerminated rice. The extract contained considerable amounts of antioxidantβ-carotene (414±12 ng/g of extract) and phytochemicals such as total polyphenols (12.0±1.1 mg gallic acid equivalent/g of extract) and flavonoids (11.0±1.4 mg catechin equivalent/g of extract). The antioxidant potential of the extract was assessed by its DPPH- (2,2-diphenyl-1-picrylhydrazyl-) free radical scavenging activity where we observed that germosprout extract had considerable antioxidative potentials. To evaluate antihemolytic effect of the extract, freshly prepared erythrocytes were incubated with either peroxynitrite or Fenton’s reagent in the absence or presence of the extract. We observed that erythrocytes pretreated with the extract exhibited reduced degree ofin vitrohemolysis. To support the proposition that germosprout extract could act as a good antioxidative agent, we also inducedin vitrooxidative stress in erythrocyte membranes and in the aorta, brain, heart, and liver tissue homogenates in the presence of the extract. As expected, germosprout extract decreased oxidative stress almost to the same extent as that of vitamin E, as measured by lipid peroxide levels, in all the mentioned tissues. We conclude that rice germosprout extract could be a good natural source of antioxidants to reduce oxidative stress-induced hemolysis and damage of blood vessels and other tissues.

In the month of holy Ramadan, food habit of Bangladeshi Muslims grossly changed. During this period they prefer to take lots of oily fried items which might be the cause of hepatocellular injury. The study was undertaken to find out the effect of oyster mushroom (P. ostreatus) on the serum level of hepatocellular enzymes like Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST), which are the two common markers for liver function tests (LFTs). The feeding of 50 grams fresh fried oyster mushroom as ifter item in Ramadan fast significantly reduced the serum levels of AST and ALT in female subjects as compared to those with the control females. Findings of the study suggest that P. ostreatus may be hepatoprotective in females and hence the human subjects. DOI: http://dx.doi.org/10.3329/jdnmch.v17i2.12220 J. Dhaka National Med. Coll. Hos. 2011; 17 (02): 56-60

Objective: Raphanus sativus is a hugely used edible root vegetable. We investigated whether the feeding of the Raphanus sativus hot water extract (RSE) ameliorates atherogenic lipid profile and oxidative stress in hypercholesterolemia. Methods: After feeding of the RSE to hypercholesterolemic rats for 6 weeks, the levels of plasma and hepatic total cholesterol (TC), triglyceride (TG), and plasma high density lipoprotein-cholesterol (HDL-C) and fecal TC levels were studied. The effects of RSE on the hepatic enzymes, namely alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP), the levels of lipid peroxide (LPO) and liver histology were also evaluated. Results: Hypercholesterolemia increased the levels of TC and TG in the plasma and livers. The levels of ALT, AST and ALP in plasma and LPO in the liver also increased. The dietary RSE, however, significantly ameliorated the above atherogenic lipids and liver enzymes. The RSE significantly reduced the levels of LPO in the liver, suggesting an in vivo protection against of oxidative stress. The RSE also inhibited the in vitro Fenton’s reagent-induced oxidative stress, thus corroborating the in vivo anti-LPO actions of RSE. The levels of hepatic LPO were positively correlated with plasma AST (r=0.76; P

We investigated the effect of Syzygium cumini(L.) Skeels seed extract on the oxidative stress of brain cortical tissues of alcohol-treated rats. The in vitro antioxidative effect of methnolic S. cumini seed extract was initially compared with those of the buytylated hydroxyl toluene (BHT) and Vitamin C, by determining their DPPH-free radical scavenging activity. The S. cumini seed extract exhibited stronger free radical scavenging activity than those of the BHT and Vitamin C. Cortex homogenates were then directly incubated with 15% ethanol and/or Fenton’s reagent (H2O2 + Fe2SO4) to induce in vitro oxidative stress in the absence or presence of S. cumini seed extract . The S. cumini seed extract significantly reduced the levels of lipid peroxide (LPO) in the cortical homogenates. Twenty four rats were then divided into four groups: Control, S. cumini seed extract (SE)-administered, 15% ethanol-fed (EtOH) and EtOH + SE rats. The oral administration of the extract (400 mg/kg BW.day) for 8 weeks significantly (P

Background Docosahexaenoic acid (DHA, C22:6, n-3) ameliorates the memory-related learning deficits of Alzheimer's disease (AD), which is characterized by fibrillar amyloid deposits in the affected brains. Here, we have investigated whether DHA-induced inhibition of Amyloid β-peptide25-35 (Aβ25-35) fibrillation limits or deteriorates the toxicity of the human neuroblastoma cells (SH-SY5Y). Experimental methods In vitro fibrillation of Aβ25-35 was performed in the absence or presence of DHA. Afterwards, SH-SY5Y cells were incubated with Aβ25-35 in absence or presence 20 μM DHA to evaluate its effect on the Aβ25-35-induced neurotoxicity by MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide)]-redox and TUNEL (TdT-mediated dUTP-biotin nick end-labeling) assay and immunohistochemistry. The level of Aβ25-35-induced lipid peroxide (LPO) was determined in the absence or presence of oligomer-specific antibody. Fatty acid profile was estimated by gas chromatography. Results DHA significantly reduced the Aβ25-35 in vitro fibrillation, as indicated by fluorospectroscopy and transmission electron microscopy. Aβ25-35 decreased the MTT-redox activity and increased the apoptotic damage and levels of LPO when compared with those of the controls. However, when the SH-SY5Y cells were treated with Aβ25-35 in the presence of DHA, MTT redox potential significantly increased and the levels LPO decreased, suggesting an inhibition of the Aβ25-35-induced neurotoxity. DHA improved the Aβ25-35 induced DNA damage and axodendritic loss, with a concomitant increase in the cellular level of DHA, suggesting DHA protects the cell from neurotoxic degeneration. Conclusion DHA not only inhibits the in vitro fibrillation but also resists the Aβ25-35-induced toxicity in the neuronal cells. This might be the basis of the DHA-induced amelioration of Aβ-induced neurodegeneration and related cognitive deficits.

Background Amyloid β (Aβ) peptide (1–40) can cause cognitive impairment. Experimental design We investigated whether dietary preadministration of eicosapentaenoic acid (EPA) is conducive to cognition learning ability and whether it protects against the impairment of learning ability in rats infused with Aβ peptide (1–40) into the cerebral ventricle. Results Dietary EPA administered to rats for 12 weeks before the infusion of Aβ into the rat brain significantly decreased the number of reference memory errors (RMEs) and working memory errors (WMEs), suggesting that chronic administration of EPA improves cognition learning ability in rats. EPA preadministered to the Aβ-infused rats significantly reduced the increase in the number of RMEs and WMEs, with concurrent proportional increases in the levels of corticohippocampal EPA and docosahexaenoic acid (DHA) and in the DHA/arachidonic acid molar ratio. Decrease in oxidative stress in these tissues was evaluated by determining the reactive oxygen species and lipid peroxide levels. cDNA microarray analysis revealed that altered genes included those that control synaptic signal transduction, cell communication, membrane-related vesicular transport functions, and enzymes and several other proteins. Conclusion The present study suggests that EPA, by acting as a precursor for DHA, ameliorates learning deficits associated with Alzheimer's disease and that these effects are modulated by the expression of proteins involved in neuronal plasticity.

The mechanism of the effect of docosahexaenoic acid (DHA; C22:6, n-3), one of the essential brain nutrients, on in vitro fibrillation of amyloid beta (Abeta(1-42)), Abeta(1-42)-oligomers and its toxicity imparted to SH-S5Y5 cells was studied with the use of thioflavin T fluorospectroscopy, laser confocal microfluorescence, and transmission electron microscopy. The results clearly indicated that DHA inhibited Abeta(1-42)-fibrill formation with a concomitant reduction in the levels of soluble Abeta(1-42) oligomers. The polymerization (into fibrils) of preformed oligomers treated with DHA was inhibited, indicating that DHA not only obstructs their formation but also inhibits their transformation into fibrils. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (12.5%), Tris-Tricine gradient(4-20%) gel electrophoresis and western blot analyses revealed that DHA inhibited at least 2 species of Abeta(1-42) oligomers of 15-20 kDa, indicating that it hinders these on-pathway tri/tetrameric intermediates during fibrillation. DHA also reduced the levels of dityrosine and tyrosine intrinsic fluorescence intensity, indicating DHA interrupts the microenvironment of tyrosine in the Abeta(1-42) backbone. Furthermore, DHA protected the tyrosine from acrylamide collisional quenching, as indicated by decreases in Stern-Volmer constants. 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide-reduction efficiency and immunohistochemical examination suggested that DHA inhibits Abeta(1-42)-induced toxicity in SH-S5Y5 cells. Taken together, these data suggest that by restraining Abeta(1-42) toxic tri/tetrameric oligomers, DHA may limit amyloidogenic neurodegenerative diseases, Alzheimer's disease.

Female Wistar rats (100 weeks old) were divided into two groups; one group was fed a high-cholesterol diet (HC) and the other a high-cholesterol diet plus docosahexaenoic acid (HC-fed DHA rats). Fatty acid concentrations in brain tissues were analyzed by gas chromatography. In the HC-fed DHA rats, brain catalase (CAT), GSH, and glutathione peroxidase (GPx) increased in the cerebrum but not in the brainstem or cerebellum. The rate of increase was 23.0% for CAT, 24.5% for GSH, and 26.3% for GPx compared with that in the HC animals (p < 0.05). In the cerebrum of the HC-fed DHA rats, CAT and GPx increased, with an increase in the ratio of DHA to arachidonic acid. The cerebrum, unlike the other areas of the brain, seems to be more sensitive to DHA in stimulating CAT and GPx. We suggest that DHA plays an important role in inducing an antioxidative defense against active oxygen by enhancing the cerebral activities of CAT, GPx, and GSH.

The effect of industrial effluent on the oxidative stress of Puntius sophore (punti fish) tissue was investigated. Oxidative stress was determined by measuring lipid peroxide (LPO) and fatty acid profile as bioindicators. Punti fishes were collected from a river where textile mill effluent is discharged, as well as from fresh water as controls. Homogenized tissues were used for LPO, fatty acid, total cholesterol, phospholipid and protein measurements. LPO levels in both hepatic and extrahepatic tissues increased significantly in the industrial-effluent-exposed fish tissue as compared with those of the freshwater fish (control versus industrial-effluent-exposed fish: hepatic tissues, 54.0 ± 5.0 and 89.0 ± 9.0 nmol/mg protein; extrahepatic tissues, 52.0 ± 9.0 and 270 ± 16.0 nmol/mg protein). Five biologically important polyunsaturated fatty acids, docosahexaenoic acid (C22:6n-3), docosapentaenoic acid (C22:5n-3), eicosapentaenoic acid (C20:5n-3), arachidonic acid (C20:4n-6) and linolenic acid (C18:3n-3), significantly decreased, and saturated fatty acid, stearic acid (C18:0), significantly increased in the effluent-exposed fish tissue than those of the freshwater counterpart. Cholesterol level of industrial-effluent-exposed punti fish was 1.5-fold lower than those of the freshwater fish. This study thus suggests that industrial effluent poses a threat, at least partially, through oxidative insult to fish tissues. PRACTICAL APPLICATIONS The study reported here indicates that fish exposed to industrial effluent induce a greater risk of oxidative stress with a resultant increased level of lipid peroxides. Consequently, if these fish with increased oxidative species are ingested by humans, they may cause physiological problems such as cardiovascular diseases and cancer involving disruption of cellular homeostasis. Therefore, an investigation about the oxidative stress of fish tissue in terms of lipid peroxidation could be of considerable significance in Third World countries where consumers remain unaware about the quality of the fish sold in the local markets and are ignorant of the oxidative stress and its consequences. The information of the present investigation may help in providing some preliminary information about the impact of unplanned industrialization on aquatic ecosystem.

1. The effects of chitosan (CS) derived from the exoskeleton of the shrimp Macrobracium rosenbergii on bodyweight, plasma lipid profile, fatty acid composition, liver lipid peroxide (LPO) levels and plasma levels of glutamate pyruvate transaminase (GPT) were determined in normocholesterolaemic (NC) and hypercholesterolaemic (HC) Long Evans rats. 2. The NC rats were fed a diet containing 2% CS and the HC rats were fed a diet containing 2 and 4% CS for 8 weeks. Chitosan significantly reduced bodyweight gain only in HC + 4% CS rats compared with HC rats, but not in NC + 2% CS or HC + 2% CS rats. 3. Chitosan reduced plasma total cholesterol in the HC + 2% CS, HC + 4% CS and NC + 2% CS rats; however, low density lipoprotein-cholesterol decreased only in the first two groups. High-density lipoprotein-cholesterol (HDL-C) increased in the HC + 4% CS rats by 24% compared with the HC + 2% CS group and by 30% compared with HC rats; however, HDL-C did not increase in the NC + 2% CS group compared with NC rats. The level of plasma triglycerides decreased significantly only in HC + 2% CS rats compared with HC rats. 4. Chitosan significantly decreased plasma levels of arachidonic acid in the HC + 2% CS and HC + 4% CS groups, with a concurrent increase in the molar ratio of total unsaturated fatty acid (TUFA) to total saturated fatty acid (TSFA). 5. Moreover, CS increased liver LPO levels without affecting plasma levels of GPT. Liver LPO levels were positively correlated with the TUFA/TSFA molar ratio. 6. The present study suggests that dietary CS decreases the atherogenic lipid profiles of both NC and HC rats and reduces the bodyweight gain of HC rats.

The effects of cholesterol-lowering statins, which substantially benefit future cardiovascular events, on fatty acid metabolism have remained largely obscured. In this study, we investigated the effects of atorvastatin on fatty acid metabolism together with the effects of TAK-085 containing highly purified eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) ethyl ester on atorvastatin-induced n-3 polyunsaturated fatty acid lowering in SHR.Cg-Lepr

Background Identifying agents that inhibit amyloid beta peptide (Aβ) aggregation is the ultimate goal for slowing Alzheimer’s disease (AD) progression. This study investigated whether the glycoside asiaticoside inhibits Aβ1–42 fibrillation in vitro. Methods Fluorescence correlation spectroscopy (FCS), evaluating the Brownian diffusion times of moving particles in a small confocal volume at the single-molecule level, was used. If asiaticoside inhibits early Aβ1–42 fibrillation steps, more Aβs would remain free and rapidly diffuse in the confocal volume. In contrast, “weaker or no inhibition” permits a greater number of Aβs to polymerize into oligomers, leading to fibers and gives rise to slow diffusion times in the solution. Trace amounts of 5-carboxytetramethylrhodamine (TAMRA)-labeled Aβ1–42 in the presence of excess unlabeled Aβ1–42 (10 μM) was used as a fluorescent probe. Steady-state and kinetic-Thioflavin T (ThT) fluorospectroscopy, laser-scanning fluorescence microscopy (LSM), and transmission electron microscopy (TEM) were also used to monitor fibrillation. Binding of asiaticoside with Aβ1–42 at the atomic level was computationally examined using the Molegro Virtual Docker and PatchDock. Results With 1 h of incubation time for aggregation, FCS data analysis revealed that the diffusion time of TAMRA-Aβ1–42 was 208 ± 4 μs, which decreased to 164 ± 8.0 μs in the presence of asiaticoside, clearly indicating that asiaticoside inhibited the early stages Aβ1–42 of fibrillation, leaving more free Aβs in the solution and permitting their rapid diffusion in the confocal volume. The inhibitory effects were also evidenced by reduced fiber formation as assessed by steady-state and kinetic ThT fluorospectroscopy, LSM, and TEM. Asiaticoside elongated the lag phase of Aβ1–42 fibrillation, indicating the formation of smaller amyloid species were impaired in the presence of asiaticoside. Molecular docking revealed that asiaticoside binds with amyloid intra- and inter-molecular amino acid residues, which are responsible for β-sheet formation and longitudinal extension of fibrils. Conclusion Finally, asiaticoside prevents amyloidogenesis that precedes neurodegeneration in patients with Alzheimer’s disease.

We studied the effect of chronic oral exposure to lead acetate (PbA) on the sensitivity of RBC to hemolysis and whether the sensitivity could be decreased by feeding the rats with extract of medicinal mushroomGanoderma lucidum. Three groups of rats, control, PbA-exposed, andG. lucidum (Gl)+PbA,were used. PbA (3 mM) was administered via drinking water andG. lucidumextract by gavage at 300 mg/Kg BW/day for 12 weeks. Afterwards, the rats were killed and washed RBCs were subjected to hemolysis in the presence of Fenton’s reagents. Hemolysis was determined by estimating the amount of released hemoglobin. The levels of lipid peroxide (LPO) and GSH were determined from RBC membranes and whole RBCs, respectively. The levels of TNFαand LPO also were determined from hepatic tissues. The RBCs of PbA-exposed rats displayed significantly higher sensitivity to hemolysis than those of theGl+PbA rats. The levels of LPO increased and GSH decreased in the RBCs, with concomitant increases in the levels of hepatic TNFαand LPO in the PbA-exposed rats. The degree of hemolysis was significantly low in the RBCs ofGl+PbA rats, concurrently with amelioration of hepatic parameters. Finally, the study suggests that PbA-induced-hemolysis and related oxidative-toxicity might be minimized by consumption ofG. lucidum.

SUMMARY 1. In the present study, we investigated the relationship between the docosahexaenoic acid (DHA)-induced protection of learning deficit of amyloid b(1-40)-infused Alzheimer’s disease (AD) model rats and changes in synaptosomal plasma membrane fluidity of the cerebral cortex. 2. Synaptosomal membrane lateral and rotational fluidity were measured using pyrene excimer spectroscopy and fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene (DPH), respectively. 3. Avoidance learning ability, as assessed by a two-way active avoidance paradigm, decreased significantly in the AD model rats. 4. Pyrene-determined annular/non-annular fluidity ratio and the DPH-determined bulk fluidity of the synaptosomal plasma membrane decreased in the amyloid b(1-40)-infused rats. Oral pre-administration of DHA (300 mg/kg per day for 12 weeks) significantly increased both lateral and rotational fluidity. 5. The synaptosomal membrane DHA content increased and the cholesterol to phospholipid molar ratio and lipid peroxidation decreased. 6. The annular to non-annular fluidity ratio of the synaptic plasma membrane was positively correlated with total avoidance learning. 7. The present results indicate that DHA-induced alterations in synaptic plasma membrane fluidity may contribute to the synaptic plasma membrane-related functions that constitute avoidance learning-related memory in amyloid b(1-40)-infused rats.

SUMMARY 1. The effects of edible oyster mushroom Pleurotus ostreatus on plasma and liver lipid profiles and on the plasma total antioxidant status were estimated in hyper- and normocholesterolaemic Long Evans rats. 2. The feeding of 5% powder of the fruiting bodies of P. ostreatus mushrooms to hypercholesterolaemic rats reduced their plasma total cholesterol by approximately 28%, lowdensity lipoprotein‐cholesterol by approximately 55%, triglyceride by approximately 34%, non-esterified fatty acid by approximately 30% and total liver cholesterol levels by > 34%, with a concurrent increase in plasma high-density lipoprotein‐ cholesterol concentration of > 21%. However, these effects were not observed in mushroom-fed normocholesterolaemic rats. 3. Mushroom feeding significantly increased plasma fatty acid unsaturation in both normo- and hypercholesterolaemic rats. 4. Plasma total anti-oxidant status, as estimated by the oxidation of 2,2 � -azino-bis-[3-ethylbenz-thiazoline-6-sulphonic-acid], was significantly decreased in mushroom-fed hypercholesterolaemic rats, concomitant with a decrease in plasma total cholesterol. 5. The present study suggests that 5% P. ostreatus supplementation provides health benefits, at least partially, by acting on the atherogenic lipid profile in the hypercholesterolaemic condition.

Docosahexaenoic acid (C22:6, n-3), a major n-3 fatty acid of the brain, has been implicated in restoration and enhancement of memory-related functions. Because Alzheimer's disease impairs memory, and infusion of amyloid-beta (Abeta) peptide (1-40) into the rat cerebral ventricle reduces learning ability, we investigated the effect of dietary pre-administration of docosahexaenoic acid on avoidance learning ability in Abeta peptide-produced Alzheimer's disease model rats. After a mini-osmotic pump filled with Abeta peptide or vehicle was implanted in docosahexaenoic acid-fed and control rats, they were subjected to an active avoidance task in a shuttle avoidance system apparatus. Pre-administration of docosahexaenoic acid had a profoundly beneficial effect on the decline in avoidance learning ability in the Alzheimer's disease model rats, associated with an increase in the cortico-hippocampal docosahexaenoic acid/arachidonic acid molar ratio, and a decrease in neuronal apoptotic products. Docosahexaenoic acid pre-administration furthermore increased cortico-hippocampal reduced glutathione levels and glutathione reductase activity, and suppressed the increase in lipid peroxide and reactive oxygen species levels in the cerebral cortex and hippocampus of the Alzheimer's disease model rats, suggesting an increase in antioxidative defence. Docosahexaenoic acid is thus a possible prophylactic means for preventing the learning deficiencies of Alzheimer's disease.

The aim of this study was to examine the optimum time of rehabilitation initiation after stroke in terms of disabilities, mobility and fall risk assessment. Data were collected prospectively at seven tertiary level health care centers in Bangladesh during the 36 months period from 2013 to 2016. All respondents were divided into four groups based on the initiation of rehabilitation as: a) 0-24 hours, b) 25-72 hours, c) 4-7 days and d) 8-60 days. Results show that significant improvement on stroke recovery, disabilities reduction, improvement in mobility restriction and reduction of fall risks in all the four groups but more improvement was observed in 0-24 hour’s group during follow-up after 3 and 12 weeks. On multinomial logistic regression analysis, the independent factors shows the mobility restriction and fall risk were more in the younger patients, male gender, married, hemorrhagic lesion and bilateral stroke.

Objective: To assess the effects of a widely used antibiotic, oxytetracycline (OTC) on the bacterial microflora in two catfish species under artificial culture conditions in the laboratory. Methods: The experiment was conducted in the Faculty of Fisheries, Bangladesh Agricultural University, Mymensingh-2202. The fish were reared in six aquaria (size 37 cm×30 cm×60 cm) where three aquaria served as replicates of the antibiotic treatment groups and the remaining three aquaria served as an untreated control group. Each aquarium was stocked with 25 fish on an average body weight 15 g. OTC was administered to the fish in the treatment groups at the rate of 2 g/kg in-feed twice daily upto ad libitum, whereas fish in the untreated control groups were given the same feed without antibiotics for 20 d. During the experiment, bacterial loads were estimated as colony forming unit (CFU/g) by every alternate day in the aquarium water, gills, skin and intestine of fish. Results: The administration of OTC in feed resulted in gradual decrease of bacterial loads in the gills, intestine and skin of the two catfish species tested. In contrast, the bacterial loads remain unchanged or slightly increased in the control groups not fed with OTC. Water quality parameters such as dissolved oxygen, pH and total hardness were found to be within suitable range in the test aquaria but not in control aquarium throughout the experimental period. Conclusions: The results of this experiment showed that in-feed antibiotic OTC for a period of 20 d reduced the bacterial loads in the gills, intestines and skin of treated fish.

We investigated whether a highly purified eicosapentaenoic acid (EPA) and a concentrated n-3 fatty acid formulation (prescription TAK-085) containing EPA and docosahexaenoic acid (DHA) ethyl ester could improve the learning ability of aged rats and whether this specific outcome had any relation with the brain levels of EPA-derived eicosanoids and DHA-derived docosanoids. The rats were tested for reference memory errors (RMEs) and working memory errors (WMEs) in an eight-arm radial maze. Fatty acid compositions were analyzed by GC, whereas brain eicosanoid/docosanoids were measured by LC–ESI-MS–MS-based analysis. The levels of lipid peroxides (LPOs) were measured by thiobarbituric acid reactive substances. The administration of TAK-085 at 300 mg·kg− 1 day− 1 for 17 weeks reduced the number of RMEs in aged rats compared with that in the control rats. Both TAK-085 and EPA administration increased plasma EPA and DHA levels in aged rats, with concurrent increases in DHA and decreases in arachidonic acid in the corticohippocampal brain tissues. TAK-085 administration significantly increased the formation of EPA-derived 5-HETE and DHA-derived 7-, 10-, and 17-HDoHE, PD1, RvD1, and RvD2. ARA-derived PGE2, PGD2, and PGF2α significantly decreased in TAK-085-treated rats. DHA-derived mediators demonstrated a significantly negative correlation with the number of RMEs, whereas EPA-derived mediators did not exhibit any relationship. Furthermore, compared with the control rats, the levels of LPO in the plasma, cerebral cortex, and hippocampus were significantly reduced in TAK-085-treated rats. The findings of the present study suggest that long-term EPA + DHA administration may be a possible preventative strategy against age-related cognitive decline.