Nicotine exacerbates liver damage in a mice model of Ehrlich ascites carcinoma through shifting SOD/NF-κB/caspase-3 pathways: ameliorating role of Chlorella vulgaris.

Nicotine, a pervasive global environmental pollutant, is released throughout every phase of the tobacco's life cycle. This study examined the probable ameliorative role of Chlorella vulgaris (ChV) extract against nicotine (NIC)-induced hepatic injury in Ehrlich ascites carcinoma (EAC) bearing female Swiss mice. Sixty female Swiss mice were assigned to four equal groups orally gavaged 2% saccharin 0.2 mL/mouse (control group), orally intubated 100 mg ChV /kg (ChV group), orally intubated 100 µg/mL NIC in 2% saccharin (NIC group), and orally intubated NIC + ChV as in group 3 and 2 (NIC+ChV group). The dosing was daily for 4 weeks. Mice from all experimental groups were then inoculated intraperitoneally with viable tumor cells 2.5 × 106 (0.2 mL/mouse) in the fourth week, and the treatments were extended for another 2 weeks. The results have shown that NIC exposure significantly altered the serum levels of liver function indices, lipid profile, LDH, and ALP in the NIC-exposed group. NIC administration significantly increased hepatic inflammation, lipid peroxidation, and DNA damage-related biomarkers but reduced antioxidant enzyme activities. NIC exposure downregulated SOD1, SOD2, CAT, GPX1, and GPX2 but upregulated NF-κB hepatic gene expression. Notably, the presence of the EAC cells outside the liver was common in all mice groups. Liver tissue of the NIC-exposed group showed multifocal expansion of hepatic sinusoids by neoplastic cells. However, with no evidence of considerable infiltration of EAC cells inside the sinusoids or in periportal areas in the NIC + ChV groups. NIC significantly altered caspase-3, Bax, and BcL2 hepatic immune expression. Interestingly, ChV administration significantly mitigates NIC-induced alterations in hepatic function indices, lipid profile, and the mRNA expression of antioxidant and NF-κB genes and regulates the caspase-3, Bax, and BcL2 immunostaining. Finally, the in vivo protective outcomes of ChV against NIC-induced hepatic injury combined with EAC in female Swiss mice could suggest their helpful role for cancer patients who are directly or indirectly exposed to NIC daily.

Thymol abates the detrimental impacts of imidacloprid on rat brains by lessening oxidative damage and apoptotic and inflammatory reactions.

Imidacloprid (IMID) is one of the most widely used neonicotinoid insecticides globally and, consequently, a probable widespread environmental contaminant. The potential neurotoxic effects of IMID have been previously reported. This study aimed to investigate the possible beneficial effect of thymol (TML) in relieving IMID-induced harmful effects on the brain of male Sprague-Dawley rats. For this aim, four groups (10 rats/group) were orally administered corn oil, TML (30 mg/kg b.wt), IMID (22.5 mg/kg b.wt), or TML + IMID for 56 days. The brain tissues were biochemically, histopathologically, and immunohistochemically evaluated. The results displayed that TML significantly restored the IMID-induced depletion of the total antioxidant capacity of the brain tissues. At the same time, the IMID-associated increased levels of lipid peroxidation in terms of malondialdehyde content were markedly suppressed in the TML + IMID group. Also, TML oral dosing markedly reduced the release of inflammatory elements, including nitric oxide and myeloperoxidase, resulting from IMID exposure. Furthermore, the IMID-induced decrease in gamma-aminobutyric acid but the increase in acetylcholinesterase was considerably reversed by TML oral dosing. Additionally, TML oral administration significantly counteracted the IMID-induced brainepatic DNA damage, as revealed by the comet assay. Besides, a significant downregulatibrainepatic Caspase-3 was evident in the TML + IMID group compared to the IMID group. However, TML oral dosing has not significantly altered the IMID-induced nuclear factor (NF-κB p65) increase. Therefore, TML could be a protective agent against IMID-induced detrimental impacts on brain tissue, possibly through its antioxidant, antiapoptotic, and anti-inflammatory activities.

Dietary 1,3-ß-Glucans Affect Growth, Breast Muscle Composition, Antioxidant Activity, Inflammatory Response, and Economic Efficiency in Broiler Chickens.

Recently, researchers have been intensively looking for novel, safe antibiotic alternatives because of the prevalence of many clinical and subclinical diseases affecting bird flocks and the risks of using antibiotics in subtherapeutic doses as feed additives. The present study intended to evaluate the potential use of 1,3-ß-glucans (GLC) as antibiotic alternative growth promotors and assessed the effect of their dietary inclusion on the growth performance, carcass traits, chemical composition of breast muscles, economic efficiency, blood biochemical parameters, liver histopathology, antioxidant activity, and the proinflammatory response of broiler chickens. This study used 200 three-day-old ROSS broiler chickens (50 chicks/group, 10 chicks/replicate, with an average body weight of 98.71 ± 0.17 g/chick). They were assigned to four experimental groups with four dietary levels of GLC, namely 0, 50, 100, and 150 mg kg-1, for a 35-day feeding period. Birds fed diets containing GLC showed an identical different growth rate to the control group. However, the total feed intake (TFI) increased quadratically in the GLC50 and GLC100 groups as compared to that in the control group. GLC addition had no significant effect on the weights of internal and immune organs, except for a decrease in bursal weight in the GLC150 group (p = 0.01). Dietary GLC addition increased the feed cost and total cost at 50 and 100 mg kg-1 doses. The percentages of n-3 and n-6 PUFA in the breast muscle of broiler chickens fed GLC-supplemented diets increased linearly in a dose-dependent manner (p < 0.01). The serum alanine aminotransferase (ALT) level and the uric acid level were quadratically increased in the GLC150 group. The serum levels of total antioxidant capacity, catalase, superoxide dismutase, interleukin-1ß, and interferon-gamma linearly increased, while the MDA level decreased in the GLC-fed groups in a dose-dependent manner. Normal histological characterization of different liver structures in the different groups with moderate round cells was noted as a natural immune response around the hepatic portal area. The different experimental groups showed an average percentage of positive immunostaining to the proinflammatory marker transforming growth factor-beta with an increase in the dose of GLC addition. The results suggest that GLC up to 100 mg kg-1 concentration can be used as a feed additive in the diets of broiler chickens and shows no adverse effects on their growth, dressing percentage, and internal organs. GLC addition in diets improves the antioxidant activity and immune response in birds. GLC help enrich the breast muscle with n-3 and n-6 polyunsaturated fatty acids.

A Preliminary Study on the Effect of Psyllium Husk Ethanolic Extract on Hyperlipidemia, Hyperglycemia, and Oxidative Stress Induced by Triton X-100 Injection in Rats.

The aim of this study is to assess the efficiency of psyllium husk ethanolic extract (PHEE) on Triton X-100 induced hyperlipidemic rats by studying the changes in hepatic and pancreatic function and histopathology. Forty male albino rats (bodyweight 175-188 g) were grouped randomly into four sets with ten rats. The experimental groups included: (1) control group (CON); (2) Triton X-100 induced hyperlipidemic group-rats were intraperitoneally injected with a single dose of Triton X-100 (100 mg/kg body weight) on the 21st day of Trial onset; (3) PHEE group-PHEE was orally administered (100 mg/kg body weight dissolved in 1 mL of distilled water) by gastric tube from the first day of the experiment until the fortieth day, once daily, (PHEE); (4) PHEE +Triton group, which received PHEE orally with the induction of hyperlipidemia. Treating hyperlipidemic rats with PHEE showed a decrease in the total serum lipids, triglyceride (TG), total cholesterol (TC), atherogenic index (AI), and malondialdehyde (MDA) with an increase in superoxide dismutase (SOD) and catalase (CAT) activities. PHEE administration alleviated the negative impact of Triton on the serum levels of glucose, insulin, glycated hemoglobin (HbA1c), homeostatic model assessment for insulin resistance (HOMA IR index), leptin hormone, Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST), Gamma-Glutamyl Transferase (GGT) and proteinogram. The Triton-induced hyperlipidemic rats showed extensive histopathological changes in the liver and pancreas, which were alleviated with PHEE administration. It could be concluded that PHEE has potent effects against hyperlipidemia, hyperglycemia, and oxidative stress due to its biologically active constituents detected by GC-MS analysis. This study's findings may help develop a novel trial against the effects of hyperlipidemia in the future.