Evaluation of anti-cancer effects of carnosine and melittin-loaded niosomes in MCF-7 and MDA-MB-231 breast cancer cells.

Background: We investigated the anti-cancer effect of carnosine-loaded niosomes (Car-NIO) and melittin-loaded niosomes (Mel-NIO) with olaparib in breast cancer cell lines (MCF-7 and MDA-MB-231). Methods: The thin film method was used for preparing the niosomes and characterized in terms of morphology, size, and polydispersity index (PDI). We further evaluated the impact of these peptides on breast cancer cells viability, RT-qPCR assays, malondialdehyde (MDA) activity, and cell cycle progression, to determine if these are linked to carnosine and melittin's anti-proliferative properties. Results: Car-NIO and Mel-NIO in vitro study inhibited cancer cell viability. They have also upregulated the expression of protein 53 (P53), BCL2-Associated X Protein (Bax), caspase-9, caspase-3, programmed cell death 4 (PDCD4), and Forkhead box O3 (FOXO3), while downregulated the expression of B-cell lymphoma 2 (Bcl2), poly (ADP-ribose) polymerase (PARP 1), and MicroRNA-183 (miRNA-183). The MCF-7 cells were arrested at the G2/M phase in Car-NIO, on the other hand, the MDA-MB-231 cells were arrested at the S phase. While the Mel-NIO and olaparib arrested the MCF-7 and MDA-MB-231 cells at the G0/1 phase. Conclusion: Our study successfully declared that Mel-NIO had more anti-cancer effects than Car-NIO in both MCF-7 and MDA-MB-231 breast cancer cells.

Palliative Effect of Resveratrol against Nanosized Iron Oxide-Induced Oxidative Stress and Steroidogenesis-Related Genes Dysregulation in Testicular Tissue of Adult Male Rats.

The nano-sized iron oxide (Fe2O3-NPs) is one of the most used engineered nanomaterials worldwide. This study investigated the efficacy of natural polyphenol resveratrol (RSV) (20 mg/kg b.wt, orally once daily) to alleviate the impaired sperm quality and testicular injury resulting from Fe2O3-NPs exposure (3.5 or 7 mg/kg b.wt, intraperitoneally once a week) for eight weeks. Spermiograms, sexual hormonal levels, oxidative stress indicators, and lipid peroxidation biomarker were assessed. Moreover, the steroidogenesis-related genes mRNA expressions were evaluated. The results showed that RSV substantially rescued Fe2O3-NPs-mediated sperm defects. Additionally, the Fe2O3-NPs-induced depressing effects on sperm motility and viability were markedly counteracted by RSV. Moreover, RSV significantly restored Fe2O3-NPs-induced depletion of testosterone, follicle-stimulated hormone, luteinizing hormone, and testicular antioxidant enzymes but reduced malondialdehyde content. Furthermore, the Fe2O3-NPs-induced downregulation of steroidogenesis-related genes (3 ß-HSD, 17 ß-HSD, and Nr5A1) was significantly counteracted in the testicular tissue of RSV-treated rats. These findings concluded that RSV could limit the Fe2O3-NPs-induced reduced sperm quality and testicular injury most likely via their antioxidant activity and steroidogenesis-related gene expression modulation.

The ameliorative effect of curcumin on hepatic CYP1A1 and CYP1A2 genes dysregulation and hepatorenal damage induced by fenitrothion oral intoxication in male rats.

This research aimed to assess curcumin (CUR) effects on fenitrothion (FNT), a broad-spectrum organophosphate insecticide, -induced hepatorenal damage. Thirty adult male Wistar rats were allocated at random to five equal groups orally administered distilled water containing 1% carboxyl methylcellulose, corn oil (1 mL/rat), CUR (100 mg/kg b.wt.), FNT (5 mg/kg b.wt.), or CUR + FNT. CUR and FNT were dosed three times a week for two months. At the end of this trial, blood and tissue samples (liver and kidney) were subjected to molecular, biochemical, and histopathological assessments. The results revealed that CUR significantly diminished the FNT-induced up-regulation of hepatic CYP1A1 and CYP1A2 transcriptional levels. Moreover, CUR significantly suppressed the increment of the serum levels of hepatic alanine aminotransferase, gamma-glutamyl transferase, and kidney damage indicators (urea and creatinine) in FNT-intoxicated rats. Furthermore, in the hepatic and renal tissues, CUR remarkably restored the FNT-associated depletion of the antioxidant enzymes (glutathione peroxidase, glutathione reductase, glutathione S transferase, catalase, and superoxide dismutase). In addition, CUR notably reduced the FNT-induced increment in malondialdehyde content in the hepatic and renal tissues. Besides, the pathological aberrations in liver and kidney tissues resulting from FNT exposure were significantly abolished in FNT + CUR treated rats. Overall, CUR could be an effective ameliorative agent against negative pesticide impacts like FNT.

Autophagy Promotes the Survival of Adipose Mesenchymal Stem/Stromal Cells and Enhances Their Therapeutic Effects in Cisplatin-Induced Liver Injury via Modulating TGF-ß1/Smad and PI3K/AKT Signaling Pathways.

Autophagy is a key metabolic process where cells can recycle its proteins and organelles to regenerate its own cellular building blocks. Chemotherapy is indispensable for cancer treatment but associated with various side-effects, including organ damage. Stem cell-based therapy is a promising approach for reducing chemotherapeutic side effects, however, one of its main culprits is the poor survival of transplanted stem cells in damaged tissues. Here, we aimed to test the effects of activating autophagy in adipose-derived mesenchymal stem/stromal cells (ADSCs) on the survival of ADSCs, and their therapeutic value in cisplatin-induced liver injury model. Autophagy was activated in ADSCs by rapamycin (50 nM/L) for two hours before transplantation and were compared to non-preconditioned ADSCs. Rapamycin preconditioning resulted in activated autophagy and improved survival of ADSCs achieved by increased autophagosomes, upregulated autophagy-specific LC3-II gene, decreased protein degradation/ubiquitination by downregulated p62 gene, downregulated mTOR gene, and finally, upregulated antiapoptotic BCL-2 gene. In addition, autophagic ADSCs transplantation in the cisplatin liver injury model, liver biochemical parameters (AST, ALT and albumin), lipid peroxidation (MDA), antioxidant profile (SOD and GPX) and histopathological picture were improved, approaching near-normal conditions. These promising autophagic ADSCs effects were achieved by modulation of components in TGF-ß1/Smad and PI3K-AKT signaling pathways, besides reducing NF-κB gene expression (marker for inflammation), reducing TGF-ß1 levels (marker for fibrosis) and increasing SDF-1 levels (liver regeneration marker) in liver. Therefore, current results highlight the importance of autophagy in augmenting the therapeutic potential of stem cell therapy in alleviating cisplatin-associated liver damage and opens the path for improved cell-based therapies, in general, and with chemotherapeutics, in particular.

Amelioration of titanium dioxide nanoparticle reprotoxicity by the antioxidants morin and rutin.

The present study aimed to examine the ameliorative effects of morin and rutin on the reproductive toxicity induced by titanium dioxide nanoparticles (TiO2NPs) in male rats. A total of seventy adult male Sprague-Dawley rats were randomly divided into seven groups, each comprising ten rats. Nanoreprotoxicity was induced by treating rats with TiO2NPs at a dosage of 300 mg/kg body weight for 30 days. Morin (30 mg/kg body weight) and rutin (100 mg/kg body weight) were co-administered with or without TiO2NPs to rats either individually or combined. Only distilled water was administered to the control group. The results showed that TiO2NPs enhanced oxidative stress, indicated by reduced levels of antioxidants such as superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) in testicular tissues, and increased levels of the lipid peroxidation marker malondialdehyde (MDA). TiO2NPs significantly reduced the levels of sex hormones (testosterone, FSH, and LH), reduced sperm motility, viability, and sperm cell count, and increased sperm abnormalities, in addition to damaging the testicular histological architecture. TiO2NPs resulted in the downregulation of 17ß-HSD and the upregulation of proapoptotic gene (Bax) transcripts in the testicular tissues. Conversely, morin and/or rutin had a protective effect on testicular tissue. They effectively counteracted TiO2NP-induced oxidative damage and morphological injury in the testis by conserving the endogenous antioxidant mechanisms and scavenging free radicals. Thus, we suggest that morin and rutin could be used to alleviate the toxicity and oxidative damage associated with TiO2NP intake.

Morin ameliorates the testicular apoptosis, oxidative stress, and impact on blood-testis barrier induced by photo-extracellularly synthesized silver nanoparticles.

Silver nanoparticles (AgNPs) have been widely produced for different industrial purposes. Recently, biogenic synthesis of AgNPs has emerged although the extent of effects from exposure, oral exposure in particular, to nanomaterials synthesized in such a manner remains elusive. The main objective of this study was to evaluate the effects of oral administration of a dose of 50 mg/Kg body weight AgNPs biosynthesized in baker's yeast (Saccharomyces cerevisiae) over a period of eight weeks on the reproductive performance and the possibility of a protective effect through co-administration of morin. Forty-eight male Sprague-Dawley rats were used in four experimental groups (control, morin-treated group, AgNP-treated, and AgNP + morin co-treatment). AgNPs produced no significant alteration in daily food intake or body weight. Both the absolute and relative testicular weights were significantly reduced but not the epididymal weight. Also, serum levels of urea, creatinine, uric acid, and liver enzymes were significantly elevated. Furthermore, AgNPs significantly downregulated the hypothalamic-pituitary-gonadal axis. This corresponds to lower motility and viability percent, reduced sperm concentration, and a higher abnormality ratio as well as a prominent alteration in the blood-testis barrier (BTB) and testicular histology and induction of testicular apoptosis and oxidative stress. The supplementation of morin evidently restored most of the reproductive characters to its physiological range. We can conclude that exposure to the biologically synthesized AgNPs for an extended period of time has proven to be a health risk that can be ameliorated via oral administration of some bioactive agents including morin.

Endosulfan toxicity in Nile tilapia (Oreochromis niloticus) and the use of lycopene as an ameliorative agent.

OBJECTIVES: Endosulfan is a broad-spectrum organochlorine insecticide that has been commercially in use for decades to control insect pests and has been found to pollute the aquatic environment. The current study was carried out to investigate the toxic effects of endosulfan, an organochlorine pesticide, on Nile tilapia (Oreochromis niloticus), a freshwater fish, and the alleviating effects of lycopene on the induced toxicity. METHODS: Four treatment groups of fish were investigated (3 replicates of 15 fish for each group): (1) a control group, (2) a group exposed to endosulfan, (3) a group that was fed on a basal diet supplemented with lycopene, and (4) a group that was fed on a basal diet supplemented with lycopene and exposed to endosulfan. The experiment was carried out over a 4-week period. RESULTS: Endosulfan negatively affected liver function, including liver enzymes and plasma proteins. Endosulfan affected blood parameters of fish and reduced the counts of red blood cells (RBCs) and white blood cells (WBCs), as well as affected immunological parameters. Endosulfan caused oxidative stress, as it decreased the values of antioxidants catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX), and glutathione (GSH), and increased the level of lipid peroxide malondialdehyde (MDA). Additionally, endosulfan increased cytochrome P450 (CYP450) levels, while it decreased glutathione S-transferase (GST) mRNA transcript levels and distorted the normal histological structure of the liver, gills, and spleen of affected fish. Conversely, lycopene partially restored the aforementioned parameters when administered concomitantly with endosulfan. CONCLUSION: The results showed the beneficial effects of supplementing fish diets with lycopene as a natural antioxidant for ameliorating the toxicity caused by endosulfan.

Effects of clove (Syzygium aromaticum) oil on quail growth, carcass traits, blood components, meat quality, and intestinal microbiota.

To provide a safe growth promoter, the present study has investigated the effects of different levels of cold-pressed clove oil (CCPO) on growth performance, carcass traits, blood biochemistry, and intestinal microbial population of growing Japanese quails. A total of 300 quails (1-wk old) were randomly divided into 3 treatment groups: control basal diet, basal diet +0.75 mL oil/kg diet, and basal diet +1.5 mL oil/kg diet. Quails fed with 1.5 mL clove oil/kg diet showed a 3.43% improvement in live body weight vs. control group. Similar trend was observed for daily body weight gain. Feed intake gradually increased (P < 0.01) with an increase in clove oil level. The best feed conversion rate was reported for the control group, followed by the group treated with 1.5 mL CCPO/kg diet during the whole period (1 to 6 wk of age). Total globulin differed significantly in 1.5 mL CCPO/kg diet group. Antioxidant enzyme activities, lipid profile, and reduced glutathione concentrations significantly improved in a dose-dependent manner. Blood urea nitrogen, creatinine, malondialdehyde, 8-hydroxy-2΄-deoxyguanosine, and protein carbonyl levels significantly decreased in quails supplemented with 1.5 mL CCPO/kg diet vs. control group. Serum levels of insulin-like growth factor-1, insulin, growth hormone, and thyroxine significantly increased in quails supplemented with 1.5 mL CCPO/kg diet vs. control group. The intestinal bacterial population, coliforms, Escherichia coli, and Salmonella spp. in the ileal content were lower (P < 0.05) in groups treated with oil (1.5 mL/kg) vs. control group. Thus, dietary supplementation with antimicrobial CCPO (1.5 mL/kg diet) could enhance growth performance, improve health status, and reduce intestinal pathogens in Japanese quails.

Ascorbic acid protects male rat brain from oral potassium dichromate-induced oxdative DNA damage and apoptotic changes: the expression patterns of caspase-3, P 53, Bax, and Bcl-2 genes.

Our study designed to study the potential of potassium dichromate (K2Cr2O7) oral exposure to induce damage in male rat brain and to compare the possible protective role of vitamin C (VC) either pre and/or concurrent supply against (K2Cr2O7) induced changes. Thirty male rats were divided into five groups. First control group received distilled water (C), second received 120 mg/kg b.wt (VC), third received 25 mg/kg b.wt K2Cr2O7 (Cr), fourth group received VC together with K2Cr2O7 by the same former doses (VC + Cr), and the fifth group received the same oral doses of VC 2 weeks prior to and along with K2Cr2O7 for 6 weeks (VC + Cr pro/co treated). The obtained results revealed that K2Cr2O7 induced a significant decrease in cholinergic activity, glutathione reductase GR activity, reduced glutathione content GSH and ATP levels. Furthermore, K2Cr2O7 induced a significant increase in oxidative DNA damage indicated by 8-hydroxy 2'-deoxyguanosine (8OH2'dG) and formation of apoptotic DNA ladders, significant increase in malondialdehyde (MDA), protein carbonyl, and lactate dehydrogenase enzyme. Increased mRNA expression of pro-apoptotic genes, including caspase-3, p53, and Bax, unlike Bcl-2 expression, was decreased. K2Cr2O7 increased caspase-3 and decreased Bcl-2 immuno-labeling. VC supply noticeably ameliorates K2Cr2O7-induced changes which were more significantly in VC pro and concurrent supplement rather than VC concurrent supply only. Finally, it is concluded that K2Cr2O7 oral administration induced oxidative apoptotic changes in rat brain and confirms the usefulness of VC pre and concurrent supply for the amelioration of K2Cr2O7-induced events more significantly than VC concurrent supply only.

Improving growth performance and health status of meat-type quail by supplementing the diet with black cumin cold-pressed oil as a natural alternative for antibiotics.

Using antibiotics in poultry diets as growth promoters was reported to have harmful effects on consumers, so the current study was done to monitor the impact of dietary supplementation of antimicrobial black cumin oil (BCO) on carcass traits, growth performance, biochemical components, and ileal microbial populations of growing Japanese quails. Three hundred growing Japanese quails were used with three different treatments (0, 0.50, and 1.0 g BCO/g diet). Birds fed diet supplemented with 0.5 g BCO/kg diet showed significant increase in body weight comparing with the control and other treatment group. The daily feed intake and feed conversion ratio were significantly increased side by side with increasing BCO level in the diet. The majority of carcass characteristics were maximized by supplementing the quail diet with 0.5 g BCO/kg. Moreover, liver functions, anti-oxidative capacity, lipid profile and anabolic hormones showed significant improvement in BCO-treated diets in a dose-dependent manner. The BCO showed highest antibacterial effect against Escherichia coli and Salmonella enterica. The ileal bacterial populations, i.e., total bacterial count (TBC), coliform, Salmonella species, and Escherichia coli were decreased in birds supplemented with BCO 0.5 and 1.0 BCO g/kg compared with the control diet. Based on the aforementioned results, conclusion could be drawn that supplementing quail with BCO in their diet could improve productive performance traits and enhance health aspect of the birds.

Neurotoxic effects of silver nanoparticles and the protective role of rutin.

The toxicological studies on silver nanoparticles (Ag-NPs) have become a hot topic over the past few decades due to their unique properties on the nanoscale and widespread in many commercial products that launched into the market recently. This study was undertaken to shed light on Ag-NPs toxicity on neurotransmitters with special emphasis on the impact of concurrent administration of rutin with Ag-NPs in the experimental rats. The oral administration of Ag-NPs in rats induced brain oxidative stress, significant alterations in neurotransmitters and amino acids. Furthermore, transcriptional levels of glutamatergic N-methyl-d-aspartate (NMDA) receptors, monoamino oxidases (MAO-A, MAO-B) and metallothionein-III (MT-III) showed a significant elevation in Ag-NPs intoxicated rats. Moreover, histological examinations revealed astrogliosis and demyelination of neurons concomitant with neuronal degeneration and vacuolation. Strikingly, oral administration of rutin counterbalanced the toxic effects triggered by Ag-NPs. Taken together, our findings suggested that oral administration of Ag-NPs induced neurotoxicity in rats and rutin mitigates these effects.

New insight on using aged garlic extract against toxic impacts of titanium dioxide bulk salt triggers inflammatory and fibrotic cascades in male rats.

The efficacy of aged garlic extract (AGE) in alleviating the hepatic inflammation and pulmonary fibrotic responses induced by titanium dioxide (TiO2) toxicity was studied. The control group received distilled water. AGE-treated group received AGE (2ml/kgbw). TiO2- intoxicated group received TiO2 (5g/kgbw). AGE combined with TiO2 treated group administered AGE prior TiO2 by six hours at the same previously doses. All treatments were given orally every other day for two months. TiO2- intoxicated rats elicited a significant up-regulation in hepatic TLR-2, TLR-4, NF-ĸB/p65, CYP1B1 and CYP2B1 with pulmonary MMP-9, TIMP-1, TGF-ß1, collagen-1α, fibronectin mRNA. Moreover, a significant elevation in serum AST, ALT, LDH, ß-glucuronidase, N-acetyl ß glucosaminidase, hydroxyproline, MMP-9, TIMP-1, fibronectin, TGF-ß1 levels with a significant decrease in total protein that ensued from TiO2 toxicity. The ultra-histopathological findings reinforced these results. The co-administration of AGE and TiO2 alleviated these changes. These data support the nutraceutical role of AGE against TiO2 toxicity.

Effect of resveratrol and rosuvastatin on experimental diabetic nephropathy in rats.

The development of diabetic nephropathy (DN) relays mainly on control of blood glucose and restrains hyperglycemic-induced oxidative stress. Hence, the effect administration of resveratrol (RSV) (5mg/kg) alone or in combination with rosuvastatin (RSU) (10mg/kg) on development and progression of diabetic nephropathy (DN) was evaluated. Oral treatment of diabetic rats with RSV alone or co-administered with RSU improved renal dysfunction indicated by a significant decrease in serum creatinine, urinary protein and urinary TGF-ß1 when compared with diabetic control rats. Also, a significant increase in body weight, relative kidney weight with a significant decrease in serum glucose and glycated hemoglobin in diabetic treated groups when compared with diabetic control group. Hyperglycemic-induced oxidative stress in diabetic control rats indicated by a significant decrease in renal activities of catalase, superoxide dismutase, glutathione peroxidase and reduced glutathione level with a significant increase in malondialdehyde levels. However, oral treatment of diabetic rats with RSV alone or co-administered with RSU improved the antioxidant status back to control values. Similarly, mRNA analysis of quantitative real time-PCR substantiated that RSV with RSU notably normalizes the renal expression of TGF-ß1, fibronectin, NF-κB/p65, Nrf2, Sirt1 and FoxO1 in the diabetic group of rats. The histopathological observations of the combined treated diabetic rats effectively protect the kidneys from hyperglycemic-induced oxidative damage. These findings confirmed the renoprotective effects of RSV with RSU treatment through improving glycemic control and attenuating oxidative stress damage in renal tissues of diabetic rats.

Lambda cyhalothrin toxicity induces alterations in lipogenic genes and inflammatory factors in rat liver.

The present study aims to elucidate the molecular basis of lambda cyhalothrin (LCT) toxicity. Thirty-two mature male albino rats were randomly classified into four equal groups. The first group was orally administered normal saline, the second group was orally administered dimethylsulfoxide (DMSO). The third group was orally administered 1/100 LD50 (6.12 mg/kg b. wt) of a commercial formulation containing 2.5% LCT (i.e., a net dose LCT corresponding to 0.15 mg/kg b. wt). The fourth group was orally administered 1/100 LD50 (0.64 mg/kg b. wt) of a pure form of LCT. The results indicated that exposure to LCT is capable of inducing an up-regulation in the mRNA expression levels of peroxisome proliferative activated receptor α and γ (PPAR α and PPAR γ), tumor necrosis factor (TNF-α), fatty acid synthase (FAS) and sterol regulatory element binding protein-1c (SREBP-1c). Additionally, our study revealed a significant increase in serum levels of ALT, AST, ALP, γGT as well as the inflammatory cytokines TNF-α and monocyte chemoattractant protein-1 (MCP-1). A significant elevation in total lipids, total cholesterol, triacylglycerol, LDL-c and leptin with a corresponding significant decrease in HDL-c was also noted. Moreover, our results depicted that LCT treatment exhibits a significant increase in hepatic MDA levels concurrent with a significant decrease in GSH levels and the activities of CAT, SOD, and GPx. An immunohistochemical investigation also revealed a strong up-regulation of hepatic FAS in the LCT treated groups. The histopathological findings were marked by evidence in support of periportal fatty changes and interstitial aggregation of round cells.

Querectin Alleviates Zinc Oxide Nanoreprotoxicity in Male Albino Rats.

Zinc oxide nanopartciles (ZnONPs) involved in advanced technologies, and their wide-scale use in consumer market makes human beings more prone to the exposure to ZnONPs. The present study was undertaken to evaluate amelioration of ZnONP-induced toxicities with querectin in male albino rats. ZnONPs-treated rats showed a significant decrease in sperm cell count, sperm motility, live and normal sperms, as well as serum testosterone level. Severe histopathological damage with a significant increase in lipid peroxidation and a decrease in antioxidant enzymes activity and the GSH level were observed in the affected testis. Relative quantitative polymerase chain reaction results showed a significant decrease in antioxidant enzymes (superoxide dismutase and catalase) and a significant decrease in 3ß-HSD, 17ß-HSD, and Nr5A1 transcripts. Rats-administered querectin along with ZnONPs showed less toxic effects on all studied reproductive traits and mRNA transcripts. Our results suggest that querectin is beneficial for preventing or ameliorating ZnONP reproductive toxicities in males.

The Th1/Th2 paradigm in lambda cyhalothrin-induced spleen toxicity: The role of thymoquinone.

This study investigates the retrofitted role of thymoquinone (TQ) in the Th1/Th2 paradigm imbalance in lambda-cyhalothrin (LCT) treated rats. Four groups of male Wistar rats were formed: Group I served as control. Group II received 5 mg TQ/(kg bw) daily. Group III received 0.6 mg LCT/(kg bw). Group IV was treated with TQ and LCT. All treatments were given orally for 10 weeks. The LCT-treated group elicited a significant increase in MDA and NO levels with up-regulation of NF-κB/p65 and pro-inflammatory genes expression and their levels. Meanwhile, GSH and immunoglobulins concentrations were markedly decreased concomitant with lessening the activities of antioxidant enzymes and anti-inflammatory cytokine genes mRNA levels. The co-administration of TQ and LCT improved the altered antioxidant enzymes activities and concentration of cytokines with attenuation of NF-κB/p65 mRNA. These data support the antioxidant role of TQ in the Th1/Th2 imbalance paradigm during LCT toxicity.

Neurotransmitters and neuronal apoptotic cell death of chronically aluminum intoxicated Nile catfish (Clarias gariepinus) in response to ascorbic acid supplementation.

Few studies have been carried out to assess the neurotoxic effect of aluminum (Al) on the aquatic creatures. This study aims to evaluate the neurotoxic effects of long term Al exposure on the Nile catfish (Clarias gariepinus) and the potential ameliorative influence of ascorbic acid (ASA) over a 180 days exposure period. Forty eight Nile catfish were divided into four groups: control group, placed in clean water, ASA exposed group (5mg/l), AlCl3 received group (28.96 µg/l; 1/20 LC50), and group received AlCl3 concomitantly with ASA. Brain tissue was examined by using flow cytometry to monitor the apoptotic cell population, HPLC analysis for the quantitative estimation of brain monoamine neurotransmitters [serotonin (5-HT), dopamine (DA), norepinephrine (NE)]. The amino acid neurotransmitters [serum taurine, glycine, aspartate and glutamine and brain gamma aminobutyric acid (GABA)] levels were assessed, plus changes in brain tissue structure using light microscopy. The concentration of Al in both brain tissue and serum was determined by using atomic absorption spectrophotometery. The Al content in serum and brain tissue were both elevated and Al exposure induced an increase in the number of apoptotic cells, a marked reduction of the monoamine and amino acids neurotransmitters levels and changes in tissue morphology. ASA supplementation partially abolished the effects of AL on the reduced neurotransmitter, the degree of apoptosis and restored the morphological changes to the brain. Overall, our results indicate that, ASA is a promising neuroprotective agent against for Al-induced neurotoxicity in the Nile catfish.

Ameliorative effects of phycocyanin against gibberellic acid induced hepatotoxicity.

Gibberellic acid (GA3) was used extensively unaware in agriculture in spite of its dangerous effects on human health. The current study was designed to investigate the ameliorative effects of the co-administration of phycocyanin with GA3 induced oxidative stress and histopathological changes in the liver. Forty male albino rats were randomly divided into four groups. Group I (control group) received normal saline for 6 weeks, Group II (GA3 treated group) received 3.85 mg/kg body weight GA3 once daily for 6 weeks, Group III (phycocyanin treated group) received Phycocyanin 200 mg/kg body weight/day for 6 weeks orally dissolved in distilled water and Group IV was treated with GA3 and phycocyanin at the same doses as groups 2 and 3. All treatments were given daily using intra-gastric intubation and continued for 6 weeks. Our results revealed significant downregulation of antioxidant enzyme activities and their mRNA levels (CAT, GPx and Cu-Zn, SOD) with marked elevation of liver enzymes and extensive fibrous connective tissue deposition with large biliary cells in hepatic tissue of GA3 treated rats, while treatment with phycocyanin improved the antioxidant defense system, liver enzymes and structural hepatocytes recovery in phycocyanin treated group with GA3. These data confirm the antioxidant potential of Phycocyanin and provide strong evidence to support the co-administration of Phycocyanin during using GA3.