Abstract:Background: The probable mechanism of an earlier reported capacity of palm oil extracts to confer protection against high dose cadmium poisoning in rats was reported in this study. Similar experimental design earlier reported by us was retained. Rats therefore were sacrificed at intervals of twelve; twenty four and forty eight hours post CdCl2 insult. Results: Oxidative stress and antioxidant status (malondialdehyde, superoxide dismutase, catalase and glutathione) were assessed in tissues (liver, kidney, heart… Show more
“…In addition to the binding of Cd to the sulfhydryl (-SH) group of the oxidative enzymes and inhibiting them, GSH depletion also renders the antioxidant enzymes inactive 36 . The current findings are consistent with those of Elkhadrag et al and Ichipi Ifukor et al 37 , 38 . Rutin, a well-known antioxidant, has been shown to have a similar effect on these antioxidant parameters 39 .…”
Cadmium is a highly neurotoxic heavy metal that disrupts membranes and causes oxidative stress in the brain. The study aimed to investigate the neuroprotective effect of gallic acid on oxidative damage in the brains of Wistar rats exposed to cadmium chloride (CdCl2). Male Wistar rats were divided into four groups of five rats each. Group 1 was administered distilled water only throughout the study. Throughout the study, Group 2 received CdCl2 alone (5 mg/kg b.w./day), Group 3 received gallic acid (20 mg/kg b.w./day), and Group 4 received CdCl2 + gallic acid (20 mg/kg). Treatments were oral with distilled water as a vehicle. The study lasted 21 days. In the brain, the activities of cholinesterase and antioxidant enzymes were evaluated, as well as the levels of reduced glutathione, malondialdehyde, neurotransmitters, Na+/K+ ATPase, myeloperoxidase activity, nitric oxide, and interleukin-6. CdCl2-induced brain impairments in experimental animals and gallic acid prevents the following CdCl2-induced activities: inhibition of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), elevated neurotransmitters (serotonin and dopamine), decreased antioxidant enzymes (superoxide dismutase, catalase), decreased glutathione, Na+/K+ ATPases, and increased MDA and neuroinflammatory markers (myeloperoxidase (MPO), nitric oxide, and interleukin-6 in the brain of experimental rats exposed to CdCl2 (p < 0.05). Taken together, the neuroprotective effects of gallic acid on CdCl2-induced toxicity in the brains of rats suggest its potent antioxidant and neurotherapeutic properties.
“…In addition to the binding of Cd to the sulfhydryl (-SH) group of the oxidative enzymes and inhibiting them, GSH depletion also renders the antioxidant enzymes inactive 36 . The current findings are consistent with those of Elkhadrag et al and Ichipi Ifukor et al 37 , 38 . Rutin, a well-known antioxidant, has been shown to have a similar effect on these antioxidant parameters 39 .…”
Cadmium is a highly neurotoxic heavy metal that disrupts membranes and causes oxidative stress in the brain. The study aimed to investigate the neuroprotective effect of gallic acid on oxidative damage in the brains of Wistar rats exposed to cadmium chloride (CdCl2). Male Wistar rats were divided into four groups of five rats each. Group 1 was administered distilled water only throughout the study. Throughout the study, Group 2 received CdCl2 alone (5 mg/kg b.w./day), Group 3 received gallic acid (20 mg/kg b.w./day), and Group 4 received CdCl2 + gallic acid (20 mg/kg). Treatments were oral with distilled water as a vehicle. The study lasted 21 days. In the brain, the activities of cholinesterase and antioxidant enzymes were evaluated, as well as the levels of reduced glutathione, malondialdehyde, neurotransmitters, Na+/K+ ATPase, myeloperoxidase activity, nitric oxide, and interleukin-6. CdCl2-induced brain impairments in experimental animals and gallic acid prevents the following CdCl2-induced activities: inhibition of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), elevated neurotransmitters (serotonin and dopamine), decreased antioxidant enzymes (superoxide dismutase, catalase), decreased glutathione, Na+/K+ ATPases, and increased MDA and neuroinflammatory markers (myeloperoxidase (MPO), nitric oxide, and interleukin-6 in the brain of experimental rats exposed to CdCl2 (p < 0.05). Taken together, the neuroprotective effects of gallic acid on CdCl2-induced toxicity in the brains of rats suggest its potent antioxidant and neurotherapeutic properties.
“…An increase in oxidative stress indicates a decrease in the antioxidant defence system. Since oxidative stress contributes meaningfully to the pathophysiology of diseases, substances that overwhelm oxidative stress might be therapeutically beneficial [19,37,41,42].…”
“…We are aware that local processors often change approach based on economic reality especially when no one watches over them. By the way, the wear and tear of the rusty cooking irons used in the heating process coupled with the locally fabricated milling machines can adulterate final products by raising heavy metal contamination known to compromise the body’s antioxidant defense system (Ichipi-Ifukor1 et al, 2022).…”
Several studies have been published on lipid lowering effect of red palm oil (RPO) with little known about health impact of differential dosage. In this study, we examined lipid profile of hyperlipidemia-induced wistar rats fed with varying quantity of RPO supplementation (15ml/kg, 20ml/kg and 25ml/kg feed). A total of 30 male wistar rats were procured and randomly divided into five groups (A, B, C, D and E) with 6 rats in each group. Group C, D and E received 15 ml/kg, 20ml/kg and 25ml/kg of RPO respectively (thoroughly mixed with high fat diet). No force feeding or oral gavage procedures were employed. While rats in group A were fed with standard rat chow, group B animals fed on high fat diet only and neither of the two groups received RPO supplementation. Plasma concentration of total cholesterol (TC), triglycerides (TG), Albumin, low density lipoproteins (LDL-C), high density lipoproteins (HDL-C), and total proteins (TP) were assessed at the end of the experiment that lasted 4 weeks. In addition to the lipid lowering effect observed in RPO supplementation groups (C, D, E) compared to fatty diet fed only (group B) as widely reported in many studies, both the LDL-C and TG appeared to rise with more RPO supplementation. Findings also revealed lipid lowering effect more pronounced on triglycerides than the low density lipoproteins. TP in group E was significantly higher compared to group A and B (P < 0.05) and RPO supplementation had a tendency to increase plasma TP.
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