Changes in the growth, ileal digestibility, intestinal histology, behavior, fatty acid composition of the breast muscles, and blood biochemical parameters of broiler chickens by dietary inclusion of safflower oil and vitamin C.

BACKGROUND: The effects of safflower oil and vitamin C (Vit. C) inclusion in broiler chicken diets on the growth performance, apparent ileal digestibility coefficient "AID%" of amino acids, intestinal histology, behavior, carcass traits, fatty acid composition of the breast muscle, antioxidant and immune status for a 35-day feeding period were evaluated. A total of 300 three-day-old Ross chicks (58.25 g ± 0.19) were randomly allotted in a 2 × 3 factorial design consisting of two levels of vitamin C (0 and 400 mg/kg diet) and three levels of safflower oil (0, 5, and 10 g/kg diet). RESULTS: An increase in the final body weight, total body weight gain, total feed intake, and the relative growth rate (P <  0.05) were reported by safflower oil and vitamin C inclusion. Dietary supplementation of safflower oil and vitamin C had a positive effect (P <  0.05) on the ingestive, resting, and feather preening behavior. Vitamin C supplementation increased (P <  0.05) the AID% of lysine, threonine, tryptophan, arginine, and valine. Safflower inclusion (10 g/kg) increased (P <  0.05) the AID% of methionine and isoleucine. Safflower oil inclusion increased (P <  0.05) the levels of stearic acid, linoleic acid, saturated fatty acids, and omega-3 fatty acids (ω-3) in the breast muscle. In contrast, the supplementation of only 10 g of safflower oil/kg diet increased (P = 0.01) the omega-3/omega-6 (ω-3/ω-6) fatty acids ratio. Vit. C supplementation increased (P <  0.05) the CAT serum levels, SOD, and GSH enzymes. Dietary supplementation of safflower oil and vitamin C improved the intestinal histology. They increased the villous height and width, crypt depth, villous height/crypt depth ratio, mucosal thickness, goblet cell count, and intra-epithelium lymphocytic lick cell infiltrations. The serum levels of IgA and complement C3 were increased (P <  0.01) by Vit. C supplementation and prominent in the 400 vit. C +  10 safflower Oil group. CONCLUSION: A dietary combination of safflower oil and vitamin C resulted in improved growth rate, amino acids AID%, intestinal histology, welfare, immune and antioxidant status of birds, and obtaining ω-3 and linoleic acid-enriched breast muscles. The best inclusion level was 400 vit. C +  10 safflower Oil.

Prevention of melamine-induced hepatorenal impairment by an ethanolic extract of Moringa oleifera: Changes in KIM-1, TIMP-1, oxidative stress, apoptosis, and inflammation-related genes.

BACKGROUND/AIMS: Melamine (ML) is a common food adulterant and contaminant. Moringa oleifera is a well-known medicinal plant with many beneficial biological properties. This study investigated the possible prophylactic and therapeutic activity of an ethanolic extract of M. oleifera (MEE) against ML-induced hepatorenal damage. METHOD: Fifty male Sprague Dawley rats were orally administered distilled water, MEE (800 mg/kg bw), ML (700 mg/kg bw), MEE/ML (prophylactically) or MEE+ML (therapeutically). Hepatic aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphate (ALP) in serum were measured. Serum total bilirubin, direct bilirubin, indirect bilirubin, protein, albumin, and globulin contents were also assayed, and urea and creatinine levels were determined. Moreover, antioxidant enzyme activity of glutathione peroxidase (GPx) and catalase (CAT) in serum levels were quantified. Complementary histological and histochemical evaluation of renal and hepatic tissues was conducted, and expression of oxidative stress (GPx and CAT) and apoptosis-related genes, p53 and Bcl-2, in hepatic tissue were assessed. In parallel, transcriptional expression of inflammation and renal injury-related genes, including kidney injury molecule 1 (KIM-1), metallopeptidase inhibitor 1 (TIMP1), and tumor necrosis factor alpha (TNF-α) in the kidney tissue were determined. RESULTS: ML caused significant increases in serum levels of ALT, AST, ALP, total bilirubin, direct bilirubin, indirect bilirubin, urea, and creatinine. Further, ML treated rats showed significant reductions in serum levels of protein, albumin, globulin, GPx, and CAT. Distinct histopathological damage and disturbances in glycogen and DNA content in hepatic and renal tissues of ML treated rats were observed. KIM-1, TIMP-1, and TNF-α gene expression was significantly upregulated in kidney tissue. Also, GPx, CAT, and Bcl-2 genes were significantly downregulated, and p53 was significantly upregulated in liver tissue after ML treatment. MEE significantly counteracted the ML-induced hepatorenal damage primarily for co-exposed rats. CONCLUSION: MEE could be an effective therapeutic supplement for treatment of ML-induced hepato-renal damage, probably via modulating oxidative stress, apoptosis, and inflammation.

Protective Effect of Curcumin against Sodium Salicylate-Induced Oxidative Kidney Damage, Nuclear Factor-Kappa Dysregulation, and Apoptotic Consequences in Rats.

This study examined the effect of sodium salicylates (SS), alone and in combination with curcumin (CUR), on kidney function and architecture in rats. Five rat groups were given 1 mL physiological saline/rat orally, 1 mL olive oil/rat orally, 50 mg CUR/kg bwt orally, 300 mg SS/kg bwt intraperitoneally, or CUR+SS for 15 days. The hematological indices, serum protein profile, serum electrolytes balance, oxidative stress, and lipid peroxidation of kidney tissues were assessed. The histopathological examination and immune expression of Caspase-3 and nuclear factor kappa (NF-κB) were conducted. The findings showed that SS injection induced nephrotoxic activity, including increased serum urea, creatinine, and uric acid levels. It also caused apparent pathological alterations with increased Caspase-3 and NF-κB immuno-expression. In addition, thrombocytopenia, leukocytosis, neutrophilia, hyponatremia, hypochloremia, hypocalcemia, and hypomagnesemia but not hyperkalemia and hyperphosphatemia were evident in SS-injected rats. Moreover, SS exposure increased serum α1 globulin, renal tissue malondialdehyde, and Caspase-3 levels but superoxide dismutase, glutathione peroxidase, and Bcl-2 levels declined. Meanwhile, CUR significantly counteracted the SS harmful impacts on kidneys but SS+CUR co-administration induced an anemic condition. Overall, CUR has an evident protective role against SS-induced renal damage, but the disturbed hematological alterations should be carefully taken into consideration in their combined use.

Boldenone Undecylenate-Mediated Hepatorenal Impairment by Oxidative Damage and Dysregulation of Heat Shock Protein 90 and Androgen Receptors Expressions: Vitamin C Preventive Role.

Boldenone Undecylenate (BLD) is a synthetic derivative of testosterone and a widely used anabolic androgenic steroid. The health risk of BLD use as a pharmaceutical or dietary supplement is still underestimated and under-reported. Vitamin C (VC) has been recognized as an antioxidant with prominent hepatorenal protective effects. This study investigated the possible preventive activity of VC against BLD-induced hepatorenal damage. Forty adult male Wistar rats were classified into five groups: control, vehicle control, VC (orally given 120 mg/kg b. wt./day), BLD (intramuscularly injected 5 mg/kg b. wt./week), and BLD + VC-treated groups. The experiment continued for eight weeks. Serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured. Serum contents of total protein (TP), albumin (ALB), globulin, total cholesterol (TC), triglycerides (TG), high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), and very-low-density lipoprotein-cholesterol (VLDL-C) were also assayed. Urea, creatinine, and uric acid levels were determined together with sodium and potassium electrolytes measuring. Moreover, oxidative stress indicators including reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and glutathione reductase (GSR) as well as malondialdehyde (MDA) levels were measured in both hepatic and renal tissues. Corresponding histological examination of renal and hepatic tissues was conducted. Besides, immunohistochemical evaluations for androgen receptors protein (AR) and heat shock protein 90 (Hsp 90) expressions were performed. BLD caused significant rises in serum ALT, AST, TP, ALB, TC, TG, LDL-C, VLDL-C, urea, creatinine, uric acid, potassium, and MDA levels. Further, BLD-injected rats showed significant declines in the serum levels of HDL-C, sodium, GSH, GPx, GST, and GSR. Besides, distinct histopathological perturbations were detected in renal and hepatic tissues of BLD-injected rats. AR and Hsp 90 immunoexpression were increased in hepatic and renal tissues. In contrast, VC significantly reversed the BLD-induced hepatorenal damage in co-treated rats but not ameliorated AR protein overexpression. VC could be an efficient preventive supplement for mitigating BLD-induced hepatorenal damage, possibly via controlling oxidative stress events.

Effects of Phenolic-Rich Onion (Allium cepa L.) Extract on the Growth Performance, Behavior, Intestinal Histology, Amino Acid Digestibility, Antioxidant Activity, and the Immune Status of Broiler Chickens.

The effect of phenolic-rich onion extract (PROE), as a feed additive, was evaluated on the growth, carcass traits, behavior, welfare, intestinal histology, amino acid ileal digestibility "AID%," and the immune status of broiler chicks for 35 days. A total number of 400, 1-day-old broiler chicks (45.38 g ± 1.35) were allocated to four different treatments with 10 replicates each (100 chicks/treatment) consisting of: T1, basal diet without additives (control treatment) (PROE0); T2, basal diet + phenolic-rich onion extract (1 g/kg diet) (PROE1); T3, basal diet + phenolic-rich onion extract (2 g/kg diet) (PROE2); and T4, basal diet + phenolic-rich onion extract (3 g/kg diet) (PROE3). An increase in the final body weight "FBW," bodyweight gain "BWG," and feed consumption was observed (P < 0.05) at different PROE levels. Also, the thymus and bursa percentages were increased in the PROE2 and PROE3 treatments (P < 0.05). The chicks fed on PROE supplemented diets had increased frequency of feeding and drinking and showed comfortable behavior (P < 0.05) with lesser aggression (P < 0.05). Additionally, an increase was observed in the antioxidant enzyme activity, phagocytic %, phagocytic index, and serum lysozyme activity in PROE supplemented treatments, with the best outcome reported in the PROE3 treatment (P < 0.01). IgM was increased in the birds fed with PROE2 and PROE3 diets (P < 0.01). PROE supplementation increased the AID% of lysine and methionine (P <0.01), PROE3 treatment increased the AID% of threonine (P < 0.05), and PROE2 and PROE3 treatments increased the AID% of leucine and isoleucine (P < 0.05). Besides, PROE2, and PROE3 treatments increased the villus height and width, mucosal thickness, and goblet cell count from the duodena, jejuna, and ilea (P < 0.05) compared to control treatment. Based on these results, we concluded that the dietary addition of phenolic-rich onion extracts can improve the growth rate of broiler chicken by improving the AID% of amino acids and intestinal histology. Also, it can improve the welfare, antioxidant enzymes activity, and immune status of the birds. Phenolic-rich onion extracts can be used as a natural growth promoter in the poultry feed for good health and improved performance.

Imidacloprid Impacts on Neurobehavioral Performance, Oxidative Stress, and Apoptotic Events in the Brain of Adolescent and Adult Rats.

Currently, imidacloprid (IMI) is the first insecticide and the second agrochemical highly applied all over the world. Here, we report on the impacts of IMI on neurobehavioral performance, oxidative stress, and apoptotic changes in the brain in either adult or adolescent rats. Forty male rats (adult and adolescent) were allocated to four groups. IMI groups were orally given 1 mg IMI/kg b.wt. dissolved in corn oil, whereas the controls were orally administered corn oil daily for 60 days. The obtained results demonstrated that IMI exposure resulted in less exploratory activity, deficit sensorimotor functions, and high depression. Levels of neurotransmitter including serotonin, gamma-aminobutyric acid, and dopamine were significantly reduced. Oxidative damage of brain tissues was evident following IMI exposure represented by the high levels of protein carbonyl, 8-hydroxyguanosine, and malondialdehyde, but total antioxidant capacity was reduced. Histopathological investigations of the brain tissues of IMI treated group revealed varying degrees of degeneration of the neuron. The immunohistochemical evaluation revealed a strong presence of glial fibrillary acidic protein (GFAP) and Bax positive cells, but a low expression of Bcl-2. These injurious impacts of IMI were very prominent in the adult rats than in the adolescent rats. Conclusively, exposure to IMI even at very low concentration could induce multiple neurobehavioral aberrations and neurotoxic impacts, especially in adults.

Assessment of protective potential of Nigella sativa oil against carbendazim- and/or mancozeb-induced hematotoxicity, hepatotoxicity, and genotoxicity.

Nigella sativa oil (NSO) possesses antioxidant activity. However, its protective role against the hazards of fungicides has been poorly studied. Therefore, the present work aimed at determining the ameliorative potential of NSO against hepatotoxicity induced by carbendazim (CBZ) and/or mancozeb (MNZ) in female rats. In the present study, about 120 adult female Sprague-Dawley rats were randomly divided into eight equal groups. One group of animals was kept as a negative control (Gp. 1); groups 2, 3 and 4 orally received CBZ (200 mg/kg body wt) and/or MNZ (300 mg/kg body wt) daily for 2 weeks (positive groups). In order to assess the hepatoprotective potential of NSO, in comparison with NSO-treated rats (Gp. 5), groups 6, 7 and 8 were CBZ- and/or MNZ-exposed groups pre-treated orally with NSO (2 ml/kg body wt) daily for 2 weeks (prophylactic groups). All groups were kept further for 15 days without medications to observe the withdrawal effect. At the end of exposure and withdrawal periods, the body weight of all experimental rats was recorded and blood samples were collected for hematological, clinico-biochemical, and micronucleus assays. The animals were then sacrificed, and the liver and bone marrow were harvested for oxidative stress bioassay, chromosomal aberrations, DNA fragmentation, and histopathological examinations. The results suggested that pre-treatment with NSO remarkably diminished CBZ- and MNZ-induced macrocytic hypochromic anemia, leukocytosis, lymphocytosis, eosinophilia, and neutropenia. Besides, it also minimized the elevated liver enzymes, lipid peroxidation, micronucleus incidence, DNA damage, and chromosomal aberration frequency. Conversely, NSO significantly stimulated the CBZ- and/or MNZ-induced antioxidant system suppression. The NSO also normalized the hepatic structural architecture. As far as withdrawal effect is concerned, there was almost disappearance of the bad effects of these fungicides and the values were close to the normal range especially with the use of NSO. Ultimately, the results revealed that N. sativa oil is an effective hepatoprotective agent due to its genoprotective and free radical scavenging activities.

Imidacloprid induces various toxicological effects related to the expression of 3ß-HSD, NR5A1, and OGG1 genes in mature and immature rats.

This study aimed to evaluate the adverse effects of the insecticide imidacloprid (IMI) on male spermatogenesis, steroidogenesis, and DNA damage in sexually mature and immature rats. Forty male rats (mature and immature) were equally divided into four groups: two mature and two immature groups. IMI groups of both ages were orally administered IMI in corn oil at a concentration of 1 mg/mL for kg BW/day, whereas their respective controls were orally administered corn oil only (1 mL/kg of body weight) daily for 65 days. On day 66, the rats were lightly anesthetized and then euthanized by cervical dislocation. Whole blood was collected for hemogram, serum for hormonal profile, semen for sperm profile, and testes for gene expression and histopathological, and immunohistochemical examinations. The obtained results revealed that both sexually mature and immature rats orally exposed to IMI showed serious abnormalities in sperm morphology and concentrations, with an imbalance of sexual hormones. There were increases in the level of serum 8-hydroxy-2'-deoxyguanosine and in the percentage of comet (tailed) sperm DNA in the IMI-treated groups. The results exhibited the upregulation of a DNA damage tolerance gene (8-oxoguanine glycosylase 1) and downregulation of the activity of steroidogenic genes (nuclear receptor subfamily 5, group A, member 1 and 3ß-hydroxysteroid dehydrogenase). Immunohistochemical examination of the B-cell lymphoma 2-associated X apoptotic protein in testicular sections showed various degrees of apoptosis in the spermatogonial cells of the IMI-treated rats compared to the control groups. These damaging effects of IMI were more pronounced in the sexually mature rats than in the immature rats. In conclusion, despite using a low dose of IMI in the present study, there were noticeable harmful consequences on the reproductive system at different stages of sexual maturity in male rats.

Protective effects of ethanolic extract of rosemary against lead-induced hepato-renal damage in rabbits.

In traditional medicine, Rosmarinus officinalis L. leaf is used as a curative herbal therapy for the treatment of several diseases. The protective effects of rosemary in toxic effects of some environmental pollutants are known. However, there is paucity of information about its protective effects on lead acetate (LD) toxicity. To assess the protection of rosemary ethanolic extracts (REE) on LD-induced hepato- and nephro-toxicity, male albino rabbits were treated with REE (30mg/kg) and/or LD (30mg LD/kg) by gavage administration for 30 days. The total phenolic compound content in REE was estimated using Folin-Ciocalteu's assay and phyto-constituents were isolated and identified using gas chromatographic and mass spectrometry (GC-MS) analysis. The protective effect of REE in LD-induced liver and renal dysfunction and blood cells was evaluated by estimating blood biomarkers of liver and renal damage, histological, and biochemical examinations. Antioxidant enzyme activities, lipid peroxidation biomarker, protein and glycogen contents were estimated in both liver and kidney homogenates. The GC-MS analysis revealed that REE is rich in phenolic compounds including camphor, phytol, borneol, caryophyllene oxide, isopulegol, thymol, and verbenone. REE pre-treatment significantly (P<0.05) suppressed levels of LD induced hepatic and renal damage products as well as lipid peroxidation. In contrast, pre-treatment using REE significantly (P<0.05) decreased LD-induced depletion of antioxidant enzymes, protein, and glycogen content. Additionally, REE preserved blood cells and their structure and renal and hepatic architecture. In conclusion, these findings revealed that REE protects from toxic effects of LD possibly through its free radical-scavenging and antioxidant activities.