Antioxidant activity and protective effect of propolis against carbon tetrachloride-induced liver and kidney injury by modulation of oxidative parameters.

BACKGROUND AND AIM: Propolis has a protective effect against cellular damage caused by toxic agents such as drugs, metals, xenobiotics, and chemicals. The aim of this study was to investigate the antioxidant activity and the effect of ethanolic extract of propolis on carbon tetrachloride (CCl4)-induced oxidative stress on kidney and liver injury in rat. MATERIALS AND METHODS: The study quantified phenol, flavone, and flavonol in propolis and assessed antioxidant activity using 2, 2-diphenyl-1-picrylhydrazyl, ferric reducing antioxidant power, and molybdate. The investigators used four groups of rats to study the effect of propolis on CCl4-induced toxicity. Propolis extract was given orally (500 mg/kg) for 12 days, and CCl4 (1 mL/kg) was administered intraperitoneally on day 5 of the experiment. Blood and tissue samples of the liver and kidney were collected on day 13 to measure biochemical and oxidative parameters. The parameters included malondialdehyde (MDA), protein carbonyl formation (PCO), advanced oxidation protein products (AOPP), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), and ascorbic acid (AA). Biochemical parameters included liver enzymes, blood urea (BU), creatinine, and uric acid (UA). RESULTS: CCl4 decreased antioxidant agents, including CAT, GPx, GSH, and AA in the liver and kidney tissues. The oxidative agents' levels, including MDA, PCO, and AOPP, increased by CCl4 compared to the control group. CCl4 increased liver enzymes, UA, BU, and creatinine in the blood samples. Propolis significantly alleviated liver and kidney function, improved antioxidant parameters, and decreased levels of oxidative agents. CONCLUSION: The data showed for the 1st time that Moroccan propolis has a protective effect against CCl4-induced kidney and liver toxicity by maintaining the activity of the antioxidant defense system, which was most likely due to its antioxidant activity.

Hepatoprotective and nephroprotective effects of sardinelle (Sardinella aurita) protein hydrolysate against ethanol-induced oxidative stress in rats.

Ethanol consumption-induced oxidative stress that is a major etiological factor has been proven to play important roles in organs' injury. In the present study, we investigated the protective effect of fish protein hydrolysate prepared from the heads and viscera of sardinelle (Sardinella aurita) (SPH) against the toxicity of ethanol on the liver and kidney of adult male rats. Animals were divided into four groups of six animals each: group C served as control, group Eth received 30 % ethanol solution at the dose of 3 g/kg body weight, group SPH received only 7.27 mg of SPH/kg body weight, and group Eth-SPH received ethanol and SPH simultaneously at the doses of 30 % and 7.27 mg/kg body weight, respectively. All groups were treated by gavage way for 15 days. Ethanol treatment decreased the defense enzymatic system including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), which increased after the co-administration of SPH. Malondialdehyde (MDA) and toxicity biomarker levels such as aspartate transaminase (AST) and alanine transaminase (ALT) and alcaline phosphatase (ALP) and gamma-glutamyl transaminase (GGT) activities were enhanced after chronic ethanol treatment and reduced by co-treatment with SPH. The histological examination of the liver and kidney confirmed biochemical changes in ethanol-treated rats and demonstrated the protective role of SPH.

Naringenin ameliorates renal and platelet purinergic signalling alterations in high-cholesterol fed rats through the suppression of ROS and NF-κB signaling pathways.

Naringenin (NGEN) is a natural flavonoid aglycone of naringin that has been reported to have a wide range of pharmacological properties, such as antioxidant activity and free radical scavenging capacity. The aim of this study was to investigate the protective effect of NGEN on oxidative and inflammatory parameters, as well as to evaluate the hydrolysis of adenine nucleotides in kidney and platelet membranes of rats exposed to a hypercholesterolemic diet (HCD) for 90 days. Kidney oxidative stress and mRNA expression of the ectonucleoside triphosphate diphosphohydrolases (NTPDases), ecto-5'-nucleotidase (CD73), inducible NO synthase (iNOS), tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6) and the nuclear factor kappa B (NF-κB) genes were evaluated by real time RT-PCR. The co-administration of NGEN (50 mg kg(-1)) for 90 days significantly prevented renal failure in HCD rats as indicated by an improvement of renal markers. Histopathological observation findings are also consistent with these effects. Moreover, NGEN (50 mg kg(-1)) significantly decreased the lipid profile and inhibited pro-oxidant and inflammation marker levels in the kidney of HCD rats. Furthermore, the NTPDase activities were significantly decreased in platelets and kidney membranes of HCD-treated rats and these alterations were improved by NGEN. In conclusion, this study suggests that naringenin can potentially improve the renal failure and platelet alterations observed in rats fed a hypercholesterolemic diet probably through its antioxidant effects.

Ability of natural astaxanthin from shrimp by-products to attenuate liver oxidative stress in diabetic rats.

BACKGROUND: Reactive oxygen species play a crucial role in the pathogenesis of diabetes and its complications. The present study was undertaken, in vivo, to examine the protective effect of astaxanthin extracted from the shell waste of deep-water pink shrimp (Parapenaeus longirostris) against oxidative stress of alloxanic adult male rats. RESULTS: Alloxan treatment revealed a significant elevation in plasma glycemia and lipid parameters such as total lipid, total cholesterol and triglycerides compared to the control group (C). In addition, liver malonaldialdehyde levels (MDA), an index of lipid peroxidation, significantly increased compared to control group. The activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) and reduced glutathione (GSH) levels decreased significantly compared to control group. Moreover, diabetic rats presented a significant increase in the activities of aspartate transaminase (AST) alanine transaminase (ALT) and alkaline phosphatase (ALP) in plasma, indicating considerable hepatocellular injury. Astaxanthin treatment restores these parameters near to control values. Histological studies on the liver tissue of alloxan and astaxanthin treated rats confirmed the protective effects of astaxanthin. CONCLUSIONS: The results revealed that astaxanthin may be helpful in preventing diabetic complications in adult rats by reversing hepatotoxicity. It can be one of the ingredients in a number of healthy products.

Astaxanthin from shrimp by-products ameliorates nephropathy in diabetic rats.

AIM: This study investigated the hypoglycemic and antioxidant effects of shrimp astaxanthin on the kidney of alloxan-induced diabetic rats. METHODS: Animals were distributed into four groups of six rats each: a control group (C), a diabetic group (D), a diabetic group supplemented with Astaxanthin (D+As) dissolved in olive oil and a diabetic group supplemented with olive oil (D+OO). In vitro antidiabetic effect was tested in plasma and kidney tissue. RESULTS: The group D of rats showed significant (P < 0.05) increase of glycemia, creatinine, urea and uric acid levels compared to those of the control group (C). Moreover, plasma and kidney malondialdehyde (MDA) and protein carbonyl (PCO) levels for the rats of the group D were significantly increased compared to the control group. Contrariwise, antioxidant enzyme activities, such as catalase (EC 1.11.1.6), superoxide dismutase (EC 1.15.1.1) and non-enzymatic levels of reduced glutathione, were significantly (P < 0.05) decreased in the plasma and kidney of diabetic rats compared to the control ones. The astaxanthin supplementation in rats diet improved the antioxidant enzyme activities and significantly decreased the MDA and PCO levels compared to diabetic rats. Indeed, no significant (P ≥ 0.05) improvement was observed for the fourth group (D+OO) compared to the control group (C). Histological analysis of kidney showed glomerular hypertrophy and tubular dilatation for the diabetic rats. For D+As rats, these histopathological changes were less prominent. CONCLUSIONS: Our results suggest that shrimp astaxanthin may play an important role in reduction of oxidative damage and could prevent pathological changes in diabetic rats suggesting promising application of shrimp astaxanthin in diabet treatment.

Founder effect confirmation of c.241A>G mutation in the L2HGDH gene and characterization of oxidative stress parameters in six Tunisian families with L-2-hydroxyglutaric aciduria.

L-2-hydroxyglutaric aciduria (L2HGA) is an autosomal recessive neurometabolic disorder characterized essentially by the presence of elevated levels of L-2-hydroxyglutaric acid (LGA) in plasma, cerebrospinal fluid and urine. L2HGA is caused by a deficiency in the L2-Hydroxyglutaric dehydrogenase (L2HGDH) enzyme involved in the oxidation of LGA to the alpha 2-ketoglutarate. LGA has been proposed as an endo- and exogenous cytotoxic organic acid that induces free radical formation and generation of reactive oxygen species (ROS). In this report, we analyzed 14 L2HGA patients belonging to six unrelated consanguineous families the south of Tunisia. The patients were diagnosed with L2HGA disease confirmed on the presence of high level of LGA in urine. We analyzed the L2HGDH gene in all probands and identified the same c.241A>G homozygous mutation, which was previously reported in Tunisia. We also used intragenic single nucleotide length polymorphisms (SNPs) and two extragenic microsatellites flanking the L2HGDH gene to confirm the founder effect of c.241A>G mutation in the 14 studied cases. In addition, we carried out the measurement of the oxidative stress parameters in the plasma of L2HGA patients which revealed a significant increase in the malondialdehyde levels (MDA), a biomarker of lipid peroxydation, and the reduced glutathione (GSH). A diminution of the antioxidant enzyme activities including superoxide dismutase (SOD), glutathione peroxidase (GPx), was also observed.

Efficacy of sardinelle protein hydrolysate to alleviate ethanol-induced oxidative stress in the heart of adult rats.

The present study was undertaken to examine the protective effects of sardinelle proteins hydrolysate (SPH) obtained from heads and viscera against ethanol toxicity in the heart of adult rats. Twenty-four male rats of Wistar strain, weighing at the beginning of the experiment 250 to 300 g, were used in this study. They were divided into 4 groups: group (C) served as controls, group (Eth) received 30% ethanol solution at 3 g/kg body weight, group (SPH) received only 7.27 mg of SPH/kg body weight, and group (Eth-SPH) received ethanol and sardinelle proteins hydrolysate simultaneously. All treatments were made by gavage during 15 d. Treatment with ethanol revealed a significant elevation of malondialdehyde and protein carbonyl levels in the heart and of aspartate transaminase and alanine transaminase activities in plasma. Nitric oxide levels and the activities of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase decreased. Nonenzymatic antioxidant such as reduced glutathione did not significantly change and ascorbic acid was decreased. SPH intake concomitantly with ethanol restored these parameters to near control values. These modifications confirmed histopathological aspects of the heart. The results revealed that SPH could provide protection of the myocardium against ethanol-induced oxidative damages in rats. This may be due to the high antioxidant potential of SPH.