Effect of garlic’s mode of administration on erythrocytes and plasma parameters in Wistar rat

Garlic preparations are recognized as hypolipidemic, cardioprotective and antihypertensive agents. However, there are some discrepancies about the beneficial effects of garlic according to dosage and mode of administration. We aimed to determine the ability of high dosage garlic (5 g/kg bw) to modulate erythrocytes and plasma parameters when administered orally (p.o.) or via intraperitoneal (i.p.) route. With regard to erythrocytes parameters, p.o. garlic treatment was found to have beneficial effects as it increased hemoglobin and hematocrit levels. Garlic i.p. treatment showed detrimental activity as it decreased these parameters. Our results reveal that garlic administered by p.o. does not involve any significant variation on mean cell volume (MCV), mean cell hemoglobin (MCH) and mean cell hemoglobin concentration (MCHC). Nevertheless, garlic i.p. increased MCV but reduced the MCH. The MCHC remained invariable even in intraperitoneal way. Concerning plasma parameters, our data show that garlic did not induce any variation on glycaemia and plasma electrolytes whatever its mode of administration. High garlic dosage was found to be relatively safe when administered orally.Keywords: Garlic, erythrocytes, hemoglobin, hematocrit, glycaemia, plasmatic electrolytes, administration mod

Protective effect of grape seed and skin extract on high dosage garlic-induced renal oxidative stress

In this study, the protective role of grape seed and skin extract (GSSE) against high garlic dose-induced renal toxicity has been evaluated. Rats were intraperitoneally injected with garlic (5 g/kg bw) or GSSE (500 mg/kg bw) or a combination of garlic and GSSE at the same doses daily for one month. Renal oxidative stress markers and antioxidant status were evaluated. We also measured plasma creatinine and urea. Data showed that high garlic dose induced renal toxicity by increasing creatinine and urea and a pro-oxidative status characterized by increased malondialdehyde, carbonyl protein, calcium and H2O2, but decreased free iron. Unexpectedly garlic increased catalase but decreased peroxidase and superoxide dismutase activities. GSSE co-treatment counteracted almost all garlic-induced deleterious effects. In conclusion, high garlic dose induced a pro-oxidative state characterized by the Fenton reaction between H2O2 and free iron, inducing Ca2+ depletion, while GSSE exerted antioxidant properties and Ca2+ repletion

Absence of Tumor Suppressor Tumor Protein 53-Induced Nuclear Protein 1 (TP53INP1) Sensitizes Mouse Thymocytes and Embryonic Fibroblasts to Redox-Driven Apoptosis

International audienceThe p53-transcriptional target TP53INP1 is a potent stress-response protein promoting p53 activity. We previously showed that ectopic overexpression of TP53INP1 facilitates cell cycle arrest as well as cell death. Here we report a study investigating cell death in mice deficient for TP53INP1. Surprisingly, we found enhanced stress-induced apoptosis in TP53INP1-deficient cells. This observation is underpinned in different cell types in vivo (thymocytes) and in vitro (thymocytes and MEFs), following different types of injury inducing either p53-dependent or-independent cell death. Nevertheless, absence of TP53INP1 is unable to overcome impaired cell death of p53-deficient thymocytes. Stress-induced ROS production is enhanced in the absence of TP53INP1, and antioxidant NAC complementation abolishes increased sensitivity to apoptosis of TP53INP1-deficient cells. Furthermore, antioxidant defenses are defective in TP53INP1-deficient mice in correlation with ROS dysregu-lation. Finally, we show that autophagy is reduced in TP53INP1-deficient cells both at the basal level and upon stress. Altogether, these data show that impaired ROS regulation in TP53INP1-deficient cells is responsible for their sensitivity to induced apoptosis. In addition, they suggest that this sensitivity could rely on a defect of autophagy. Therefore, these data emphasize the role of TP53INP1 in protection against cell injury. Antioxid. Redox Signal. 15, 1639–1653