Acrylamide is a hazardous substance inducing oxidative stress. Based on some evidence on the antioxidant properties of fenugreek, Trigonella foenum-graecum, this study was conducted to investigate the protective effect of fenugreek seed oil against acrylamide toxicity. Thirty-two male Wistar rats were randomly assigned into four groups. The control group was given normal saline. The second group was administered acrylamide (20 mg/kg bw orally). The third and fourth groups were administered acrylamide (20 mg/kg bw) and supplemented with 2.5% and 5% fenugreek seed oil in their diets, respectively. Acrylamide intoxication significantly increased serum levels of LDH, AST, ALT, APL, γ-GT, cholesterol, uric acid, urea, creatinine, 8-oxo-2'-deoxyguanosine, interleukin 1 beta, interleukin 6, and tumor necrosis factor α. Moreover, it increased hepatic, renal, and brain lipid peroxidation, while it impaired the activities and concentrations of the antioxidant biomarkers. Fenugreek oil supplementation normalized the altered serum parameters, prevented lipid peroxidation, and enhanced the antioxidant biomarker concentrations and activities in the hepatic, renal, and brain tissues of acrylamide-intoxicated rats in a dose-dependent manner. Thus, these results indicate that Trigonella foenum-graecum oil has a protective effect against acrylamide-induced toxicity through its free radical scavenging and potent antioxidant activities.

The objective of this study was to investigate the effects of Spirulina platensis powder (SPP) supplementation on growth performance, antioxidative status and blood metabolites in fattening lambs. Ten healthy lambs (46.5 ± 1.06 kg BW) were randomly assigned to one of two treatments (5 lambs per treatment) and received either no supplementation or supplemented with SPP at a rate of 1 g/10 kg BW/day. The feeding experiment was conducted for 35 days with body weight recorded and blood samples collected on days 0, 17 and 35 of the experiment. The paired Student's t-test for means was used for statistical analysis. The results showed that SPP supplementation improved final live body weight, daily live weight gain, feed intake and feed conversion ratio, compared to the control group (P<0.05). Also, haemoglobin, total white blood cell count, serum globulin, vitamin A and reduced glutathione were higher (P<0.05), while the aspartate amino transferase, alanine amino transferase, cholesterol, glucose and serum malondialdehyde levels were lower (P<0.05) in SPP supplemented group compared with the control. In conclusion, the findings of the present study clearly demonstrate that the SPP could be incorporated in fattening lambs diets as an antioxidant, immune-stimulant and growth promoter feed additive.

Age‐related cognitive failure is a main devastating incident affecting even healthy people. Alzheimer's disease (AD) is the utmost common form of dementia among the geriatric community. In the pathogenesis of AD, cerebrovascular dysfunction is revealed before the beginning of the cognitive decline. Mounting proof shows a precarious impact of cerebrovascular dysregulation in the development of AD pathology. Recent studies document that the mammalian target of rapamycin (mTOR) acts as a crucial effector of cerebrovascular dysregulation in AD. The mTOR contributes to brain vascular dysfunction and subsequence cerebral blood flow deficits as well as cognitive impairment. Furthermore, mTOR causes the blood–brain barrier (BBB) breakdown in AD models. Inhibition of mTOR hyperactivity protects the BBB integrity in AD. Furthermore, mTOR drives cognitive defect and cerebrovascular dysfunction, which are greatly prevalent in AD, but the central molecular mechanisms underlying these alterations are obscure. This review represents the crucial and current research findings regarding the role of mTOR signaling in cognitive aging and cerebrovascular dysfunction in the pathogenesis of AD.

The current study was carried out to evaluate the ameliorative effect of fucoidan against aflatoxicosis-induced hepatorenal toxicity in streptozotocin-induced diabetic rats. Sixty-four Wister albino male rats were randomly assigned into eight groups (8 rats each) that received normal saline, fucoidan (FUC) at 100 mg/kg/day orally for 4 weeks, streptozotocin (STZ) at 50 mg/kg/i.p. single dose, STZ plus FUC, aflatoxin B 1 (AFB 1 ) at 50 μg/kg/i.p. after one month of the beginning of the experiment for 2 weeks, AFB 1 plus FUC, STZ plus AFB 1 , or STZ plus AFB 1 and FUC. Injection of rats with STZ induced hyperglycemia. Rats with STZ-induced diabetes, with or without AFB 1 intoxication, had significantly elevated activities of serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase, and levels of serum urea, creatinine, cholesterol, 8-oxo-2′-deoxyguanosine, interleukin-1β, interleukin-6, and tumor necrosis factor-α. In addition, these rats exhibited increased lipid peroxidation and reduced glutathione concentration and activities of superoxide dismutase, catalase, and glutathione peroxidase enzymes in the hepatic and renal tissues. In contrast, administration of FUC to diabetic rats, with or without AFB 1 intoxication, ameliorated the altered serum parameters, reduced oxidative stress, DNA damage, and inflammatory biomarkers, and enhanced the antioxidant defense system in the hepatic and renal tissues. These results indicated that FUC ameliorated diabetes and AFB 1 -induced hepatorenal injuries through alleviating oxidative stress, DNA damage, and inflammation.