Effects of different feeding regimens with protease supplementation on growth, amino acid digestibility, economic efficiency, blood biochemical parameters, and intestinal histology in broiler chickens.

BACKGROUND: This study was conducted to estimate the impacts of using varied feeding regimens with or without protease supplementation on the growth performance, apparent amino acid ileal digestibility (AID%), economic efficiency, intestinal histology, and blood biochemical parameters of broiler chickens. Three hundred one-day-old chicks (Ross 308 broiler) were randomly allotted to a 3 × 2 factorial design. The experimental design consisted of three feeding regimens; FR1: a recommended protein SBM diet, FR2: a low-protein SBM diet, and FR3: a low-protein diet with the inclusion of 5% DDGS and 5% SFM, with or without protease supplementation (250 mg/kg). RESULTS: Increased feed intake and feed conversion ratio were observed in the FR3 treatment during the starter stage and decreased body weight and body weight gain during the grower stage. However, there was no significant effect of the different feeding regimens, protease supplementation, or interaction on the overall performance. The economic value of diets also remained unaffected by the different feeding regimens, protease supplementation, or interaction. Protease supplementation resulted in lowering the AID% of tryptophan and leucine. Reduced AID% of methionine was evident in the FR2 + VE and FR3 - VE treatments. Histological findings substantiated the FR3 treatment mediated a decrease in the duodenal and jejunal villous height (VH), jejunal villous width (VW), and ileal VW, whereas, increase in the ileal crypt depth (CD). The FR2 + VE treatment reduced the VH:CD ratio in the duodenum. The duodenal CD and the jejunal goblet cell count were reduced as a consequence of protease supplementation. The FR3 + VE treatment documented a rise in duodenal CD, while an increase in the jejunal goblet cell count was observed in the FR3 - VE treatment. The FR3 treatment enhanced the IgM serum levels compared to the FR1 and FR2 treatments. IgM serum levels were also elevated following protease supplementation. FR3 + VE treatment increased IgM serum levels. The highest serum ALP was found in the FR3 treatment, whereas the lowest level was obtained in the FR2 treatment. CONCLUSION: Low-protein SBM-based diets could be used without affecting the birds' growth. Altered morphometric measures of the intestine and increased IgM and ALP levels indicated the low-protein SBM/DDGS-SFM diet-induced damage of the intestinal histoarchitecture and immune system of birds. These different diets and protease supplementation failed to affect economic efficiency positively.

The protective efficacy of vitamin E and cod liver oil against cisplatin-induced acute kidney injury in rats.

Cisplatin (CP) is a highly effective chemotherapeutic agent against neoplasms, but its clinical utility is limited due to the side effects of its dose-dependent nephrotoxicity. Vitamin E (Vit E) and cod liver oil (CLO) are natural substances with chemoprotective effects. The present study was conducted to evaluate the protective effects of Vit E and/or CLO for CP-induced acute kidney injury (AKI) in rats. This study involved 40 mature male Wistar albino rats that were equally allocated into eight groups: Veh, Vit E, CLO, Vit E + CLO, CP, Vit E + CP, CLO + CP, and Vit E + CLO + CP. The co-administration of Vit E and CLO significantly ameliorated CP-induced elevations in serum creatinine (Cr), blood urea nitrogen (BUN), interleukin 1 beta (IL-1ß), and interleukin- 6 (IL-6). Further, rats that received Vit E and/or CLO showed significant decrease in malondialdehyde (MDA) and increases in superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) levels in renal tissues, compared to CP-intoxicated rats. Additionally, the treatment restored the normal histological architecture (except for few cast formations) and upregulated the immunostaining area% of aquaporin 3 (AQP3) and downregulated the immunostaining area% of Bcl2 associated X protein (BAX) and inducible nitric oxide synthase (iNOS). The observed effects were stronger in the combination treatment group. The obtained data revealed that Vit E and CLO co-administration protects against the CP-induced AKI more than monotherapy with Vit E or CLO.

Neurobehavioral, apoptotic, and DNA damaging effects of sub-chronic profenofos exposure on the brain tissue of Cyprinus carpio L.: Antagonistic role of Geranium essential oil.

Currently, the contamination of water with different insecticides like profenofos (PFF) is a critical concern in the aquatic ecosystem. There are limited studies available on the negative impacts of PFF on common carp fish (Cyprinus carpio L.). Therefore, the existing study was designed to investigate the effect of PFF exposure (1/10 of the 96 h-LC50) on the neurobehavior, growth performance, chemical composition, oxidative status, DNA damage, apoptotic status and histological indices of the brain and gill tissues. In addition, this study seeks to detect the ability of geranium essential oil (GEO) dietary supplementation to mitigate the negative impacts of PFF. Accordingly, a total of 120 healthy fish were divided into four groups: the control group, fed on basal diet only; the other groups were fed on a basal diet supplemented with 400 mg kg-1 GEO, basal diet and PFF in water (PFF group), and supplemented diet with GEO and PFF in water (GEO + PFF), respectively, for 60 days. The results showed that PFF significantly reduced fish growth performance, crude protein, and lipid contents. It caused several behavioral alterations including spiral movement, decreased activeness, and changes in feeding behavior. Moreover, PFF increased the DNA tail length, tail moment, and the level of 8-hydroxy-2'-deoxyguanosine. Histologically, PFF induced a wide array of circulatory, inflammatory, regressive and progressive alterations in the brain and gill tissues. PFF significantly downregulated Bcl-2 and upregulated caspase-3 immuno-expression in both organs. Further, it considerably depleted the antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase. The GEO supplementation did not reach the respective control values but markedly improved most of the behavioral, physical, biochemical, oxidative, apoptotic, and inflammatory markers, altered by PFF exposure. It also protected the gill and brain tissues from the branchial and encephalopathic effects of PFF. These findings suggest that GEO dietary supplements could be advantageous for mitigating PFF negative impacts and presenting a promising feed additive for common carp in aquaculture.

Amelioration of fenitrothion induced oxidative DNA damage and inactivation of caspase-3 in the brain and spleen tissues of male rats by N-acetylcysteine.

N-acetylcysteine (NAC) has largely been used as an effective chemo- protective agent owing to their beneficial effect in restoring several physiological parameters and relieving oxidative stress. Interestingly, it has been suggested that NAC mechanisms of action extend beyond being a precursor to the antioxidant glutathione and that they may involve several neurotropic and inflammatory pathways. Exposure to fenitrothion, an organophosphorus insecticide, promotes oxidative stress and induces several deleterious changes in the immune response and various tissues including cerebrum and spleen. The main objective of our study was to investigate ameliorative efficacy of N-acetylcysteine for immunological and neurological alterations and oxidative DNA damage induced by fenitrothion toxicity in cerebrum and spleen tissues of male rats. Our results revealed that oral exposure to fenitrothion for 30 days caused a reduction in the erythrocyte count in addition to leukocytosis, lymphocytosis, and neutrophilia. Also, this route of administration increased the serum levels of LDH, TNF-α, and IL-2 with reduction in serum immunoglobulins (IgG & IgM) concentrations. Furthermore, a significant downregulation in the antioxidant markers (GSH & SOD) with an elevation of free radical (MDA) levels were noticed. Regarding the brain, fenitrothion administration inhibited AchE activity and increased brain GABA, serotonin and dopamine levels. Moreover, it induced an elevation in oxidative DNA damage indicated by 8-hydroxy 2-deoxyguanosine (8OH2dG) and mRNA expression of pro-apoptotic genes, including Bax, and p53, but Bcl-2 expression was reduced. N-acetylcysteine co-treatment restored the normal physiological tone in most of these parameters. Immunostaining for GFAP and Caspase-3 markers in the brain and spleen tissues were increased respectively. In conclusion, N-acetylcysteine supplementation has an ameliorative effect against immunotoxic, neurotoxic and oxidative DNA damage induced by fenitrothion exposure.