Water-soluble phenolics from Phoenix dactylifera fruits as potential reno-protective agent against cisplatin-induced toxicity: pre- and post-treatment strategies.

Nephrotoxicity is the major side effect of cisplatin, an effective platinum-based chemotherapeutic drug that is applicable in the treatment of several solid-tissue cancers. Studies have indicated that certain water-soluble phenolics offer renal protection. Thus, this study investigates the role of pre and post-treatment of rats with water-soluble phenolics from Phoenix dactylifera (PdP) against nephrotoxicity induced by cisplatin. Rats were either orally pretreated or post-treated with 200 mg/kg body weight of PdP before or after exposure to a single therapeutic dose of cisplatin (5 mg/kg body weight) for 7 successive days intraperitoneally. The protective effects of PdP against Cisplatin-induced nephrotoxicity was based on the evaluation of various biochemical and redox biomarkers, together with histopathological examination of kidney tissues. The composition, structural features, and antioxidative influence of PdP were determined based on chromatographic, spectroscopic, and in vitro antioxidative models. Cisplatin single exposure led to a substantial increase in the tested renal function biomarkers (uric acid, creatinine, and urea levels), associated with an increase in malondialdehyde indicating lipid peroxidation and a significant decline (p < 0.05) in reduced glutathione (GSH) levels in the renal tissue when compared with the control group. A marked decline exists in the kidney antioxidant enzymes (catalase, SOD, and GPx). Nevertheless, treatment with PdP significantly suppressed the heightened renal function markers, lipid peroxidation, and oxidative stress. Spectroscopic analysis revealed significant medicinal phenolics, and in vitro tests demonstrated antioxidative properties. Taken together, results from this study indicate that pre- and/or post-treatment strategies of PdP could serve therapeutic purposes in cisplatin-induced renal damage.

Xylopia aethiopica suppresses markers of oxidative stress, inflammation, and cell death in the brain of Wistar rats exposed to glyphosate.

The herbicide "Roundup" is used extensively in agriculture to control weeds. However, by translocation, it can be deposited in plants, their proceeds, and the soil, thus provoking organ toxicities in exposed individuals. Neurotoxicity among others is one of the side effects of roundup which has led to an increasing global concern about the contamination of food by herbicides. Xylopia aethiopica is known to have medicinal properties due to its antioxidative and anti-inflammatory properties, and it is hypothesized to neutralize roundup-induced neurotoxicity. Thirty-six (36) Wistar rats were used for this study. The animals were shared equally into six groups with six rats each. Glyphosate administration to three of the six groups was done orally and for 1 week. Either Xylopia aethiopica or vitamin C was co-administered to two of the three groups and also administered to two other groups and the final group served as the control. Our studies demonstrated that glyphosate administration led to a significant decrease in antioxidants such as catalase, superoxide dismutase, glutathione, and glutathione peroxidase. We also observed a significant increase in inflammatory markers such as tumor necrosis factor-α, interleukin 6, C-reactive protein, and immunohistochemical expression of caspase-3, cox-2, and p53 proteins (p < 0.05). However, Xylopia aethiopica co-administration with glyphosate was able to ameliorate the aforementioned changes when compared to the control (p < 0.05). Degenerative changes were also observed in the cerebellum, hippocampus, and cerebral cortex upon glyphosate administration. These changes were not observed in the groups treated with Xylopia aethiopica and vitamin C. Taken together, Xylopia aethiopica could possess anti-oxidative and anti-inflammatory properties that could be used in combating glyphosate neurotoxicity.

D-ribose-L-cysteine exhibits neuroprotective activity through inhibition of oxido-behavioral dysfunctions and modulated activities of neurotransmitters in the cerebellum of Juvenile mice exposed to ethanol.

Alcohol exposure to the cerebellum has been known to trigger cerebellar dysfunctions through several mechanisms. This present study was designed to evaluate the repealing effect of D-ribose-L-cysteine (DRLC) on alcohol-induced cerebellar dysfunctions in juvenile BALB/c mice. The animals were randomly divided into 4 groups (n = 10 per group). Mice were given oral administration of normal saline (control), DRLC (100 mg/kg, p.o), ethanol (0.2 mL of 10% w/v), or DRLC (100 mg/kg, p.o) + ethanol (0.2 mL of 10% w/v). On day 29 of the study (i.e., 24 h after the administration of the last respective doses), neurochemical quantification of the respective levels of serotonin and dopamine, lipid peroxidation, total antioxidant, superoxide dismutase, and glutathione peroxidase in the cerebellar tissues of the mice were analyzed. Compared with the saline-treated group, the studied neurochemical indices were modulated across the various experimental groups. The administration of ethanol significantly modulates the levels of monoamine neurotransmitters (serotonin and dopamine) as well as contents of total antioxidants, activities of superoxide dismutase, and glutathione peroxidase, with a concurrently increased level of lipid peroxidase in the cerebellar tissue of the mice. DRLC significantly reverses these effects in the DRLC + ethanol co-treated group. Combined exposure to DRLC + ethanol counteracts the deleterious effect of ethanol in the cerebellum of juvenile BALB/c mice via monoamine neurotransmitter, lipid peroxidation, total antioxidant status, superoxide dismutase, and glutathione peroxidase action pathways. Therefore, DRLC could be a pharmacologic or therapeutic agent in attenuating the deleterious effects of alcohol on the cerebellum.

Mechanism underlying nephroprotective property of curcumin against sodium nitrite-induced nephrotoxicity in male Wistar rat.

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.

Curcumin protects sodium nitrite-induced hepatotoxicity in Wistar rats.

In this study, the protective effect of curcumin on sodium nitrite (NaNO2) induced hepatotoxicity was assessed in male Wistar rats. Wistar rats were administered orally daily with 20 mg/kg of curcumin for 28 days and NaNO2 was administered as a single dose of 60 mg/kg on day 28. Lipid profile, liver function biomarkers and C-reactive protein were assessed in the serum; lipid peroxidation, non-enzymatic and enzymatic antioxidants were assessed in the liver. Alanine amino transferases (94.67 U/L), aspartate amino transferases (194.33 U/L), alkaline phosphatases, C-reactive proteins (19.56 ng/L) and lipid peroxidation (8.03 × 10-6 µmol/mg protein) were significantly elevated (P < 0.05), while a significant decrease in lipid profiles (total cholesterol, HDL,LDL, and triglycerides): (0.61,0.37, 0.4 and 0.47 mg/dl respectively), reduced glutathione level (4.16 µmol/mg protein), and decreased catalase, superoxide dismutase and glutathione peroxidase activities with severe histological alterations were observed in the livers of rats exposed to NaNO2. Pre-treatment with curcumin significantly (P < 0.05) prevented these alterations by adjusting the lipid profile, liver function markers, and C-reactive proteins and abrogating the elevated markers of oxidative stress as supported by the liver histology. This suggests that dietary consumption of curcumin is beneficial against NaNO2 induced oxidative stress of the liver via its antioxidant potential.