The current work examined the outcome of curcumin (20 mg/kg body weight/day) administration on arginase and adenosine deaminase (ADA) activities and other kidney markers, as well as markers of oxidative stress, in Wistar rats exposed to sodium nitrite (NaNO₂) (60 mg/kg of body weight, single dose) for 28 days. The results revealed that the NaNO₂ exposed rats had significantly altered the ADA activities, arginase activities alongside other biomarkers of kidney function, and oxidative stress. However, pretreatment with curcumin significantly mitigated the altered activities ADA and arginase as well as other parameters. This was supported by the histopathological examination of the kidney tissues. Our findings suggest that the alteration in the activities of ADA and arginase could be involved in the mechanism of action employed by NaNO₂ and curcumin in the respective induction and prevention of nephrotoxicity. Practical applications These results suggest that moderate exposure to the acceptable daily dose of curcumin can improve food‐related kidney damage through regulations of ADA and arginase activities, enhancement in the antioxidant system, and suppression of lipid peroxidation.

Breast cancer is the most common cancer affecting women worldwide. The associated morbidity and mortality have been on the increase while available therapies for its treatment have not been totally effective. The most common treatment, chemotherapy, sometimes has dangerous side effects because of non-specific targeting, in addition to poor therapeutic indices, and high dose requirements. Consequently, agents with anticancer effects are being sought that can reduce the side effects induced by chemotherapy while increasing its cytotoxicity to cancer cells. This is possible using natural compounds that are safe and biologically active. There are many reports on plant polysaccharides due to their bioactive and anticancer properties. The use of plant polysaccharide together with a conventional cytotoxic drug may offer wide benefits in cancer therapy, producing synergistic effects, thereby reducing drug dose and, so, its associated side effects. In this review, we highlight an overview of the use of plant polysaccharides and chemotherapeutic drugs in breast cancer preclinical studies, including their mechanisms of anticancer activities. The findings emphasize the potential of plant polysaccharides to improve chemotherapeutic outcomes in breast cancer, paving the way for more effective and safer treatment strategies.

Background: Pomegranate powder derived from pomegranate fruit contains phytochemicals chief of which is ellagitannins. Owing to their high antioxidative capabilities we investigated its efficacy against lead acetate induced hepatic and renal toxicity. Methods: Pomegranate powder (500 g) was procured and soaked in 1 Litre of ethanol for three days, its filtrate was concentrated and freeze dried to form Punica granatum L. ethanol extract (PLEE). Thirty (30) male albino Wistar rats with average weight between 140 ± 20 g were used for this study. They were equally shared into 6 groups with 5 animals each; A: Control; B: Lead acetate only C: Lead acetate + PLEE (1); D: Lead acetate + PLEE (2); E: PLEE (1) and F: PLEE (2). Serum, liver and kidney samples were obtained for biochemical assays. The integrity of liver and kidney tissues were also accessed. Results: Lead administration resulted in marked elevations in liver transaminases in serum and liver as well as a significant increase in kidney function markers in the serum and kidney (p < 0.05). There was also a significant decline in average body weight, antioxidant markers in the liver and kidney of Wistar rats while there was a significant increase in lipid peroxidation levels in both liver and kidney. However, administration of PLEE at different doses significantly modulated these changes. Conclusion: Lead acetate administration led to hepatic and renal toxicity as evident by alterations in liver and kidney function markers, antioxidant status and tissue integrity. However, PLEE can combat these toxicities.

Objective: This study investigated the effect of Tridax procumbens (TP), a medicinal plant, on Vincristine sulphate (VC)-induced oxidant-antioxidant imbalances in the liver and pancreas of male Wistar rats. Methods: Thirty rats (80-100 g) were randomly allocated into six groups (Groups 1–6) and treated as follows: Group 1 (control) received 1 mL/kg body weight distilled water orally (p.o.), Group 2 received 0.1 mg/kg body weight VC intraperitoneally (i.p.), Groups 3 and 4 received 50 and 100 mg/kg body weight TP extract orally (p.o.), respectively. Group 5 received VC (0.1 mg/kg body weight, i.p.) plus TP (50 mg/kg body weight, p.o.) while Group 6 received VC (0.1 mg/kg body weight, i.p.) plus TP (100 mg/kg body weight, p.o.). The rats were treated for 10 consecutive days. Oxidant-antioxidant biomarkers and histology of the liver and pancreas of the rats were assessed. Results: Vincristine sulphate reduced the activities of Glutathione S-Transferase (GST), Glutathione Peroxidase (GPx) (p<0.05), Superoxide Dismutase (SOD) (p<0.05), and reduced glutathione (GSH) (p<0.05) levels in the liver compared to the control group, while TP administration enhanced the activities and concentrations of these antioxidant parameters. In the pancreas, VC reduced the concentration of GSH (p<0.05) and the activities of GPx and SOD compared to the control group, while TP produced opposite effects in groups exposed to TP. VC increased the contents of Malondialdehyde (MDA) (p<0.05) and hydrogen peroxide (H2O2) (p<0.05) generation and decreased total protein concentration in the liver and pancreas compared to the control group, with a counteracting effect by TP. Lastly, histological analysis of the liver exposed to VC showed moderate portal infiltration of inflammatory cells and random centrilobular degeneration, while there was more representation of islets of Langerhans and secretory acini cells in TP alone-treated rats. Conclusion: The Tridax procumbens ethanol leaf extract mitigated vincristine sulphate-induced oxidant-antioxidant imbalances in the liver and pancreas of experimental rats, thus reflecting its comparative advantage.

This study evaluated the prospective molecular and biochemical mechanisms behind the hepatoprotective effects of curcumin in Wistar rats exposed to KBrO_3. Techniques for assessment of hepatic oxidative injury and histological biomarkers were used. The concentrations of proteins connected with inflammation (e.g. tumor necrosis factor-alpha (TNF-α), interleukins 1β (IL-1β) and C-reactive protein (CRP)) were estimated by enzyme-linked immunosorbent assay (ELISA) techniques. Results showed that, curcumin administered orally at a dose of 20 mg/kg for 28 days significantly suppressed the activities of serum transaminases and alkaline induced by KBrO₃ administration (20 mg/kg, twice weekly) and protected the integrity of the liver tissue. Also, curcumin at the tested dose abridged the KBrO₃-induced increase in hepatic malondialdehyde (MDA) levels and reversed KBrO₃ mediated reduction in activities of hepatic antioxidant molecules including reduced glutathione (GSH), total thiol (TSH), glutathione peroxidase (GPx), catalase and superoxide dismutase (SOD). In addition, curcumin significantly assuaged inflammatory response in KBrO₃-lesioned liver as revealed by the decrease in inflammatory biomarkers. This study suggests that curcumin exhibits a protective effect via induction of hepatic detoxification proteins and inhibition of inflammatory proteins in addition to its antioxidative ability in KBrO₃- induced hepatic injury in rats.