Preventive supplementation with fresh and preserved peach attenuates CCl4-induced oxidative stress, inflammation and tissue damage

Abstract

The present study was elaborated to comparatively evaluate the preventive effect of different peach-derived products obtained from preserved fruits (Syrup and Preserve Pulp Peach [PPP]) and from fresh peels and pulps (Peel and Fresh Pulp Peach [FPP]) in a model of liver/renal toxicity and inflammation induced by carbon tetrachloride (CCl4) in rats. Tissue damage (carbonyl, thiobarbituric acid reactive species and sulfhydril), antioxidant enzymes activity (catalase and superoxide dismutase) and inflammatory parameters [tumor necrosis factor (TNF)-α and interleukin (IL)-1β levels, and receptor for advanced glycation end-products (RAGE) and nuclear factor (NF)κB-p65 immunocontent] were investigated. Our findings demonstrated that Peel, PPP and FPP (200 or 400 mg/kg) daily administration by oral gavage for 30 days conferred a significant protection against CCl4-induced antioxidant enzymes activation and, most importantly, oxidative damage to lipids and proteins as well as blocked induction of inflammatory mediators such as TNF-α, IL-1β, RAGE and NFκB. This antioxidant/anti-inflammatory effect seems to be associated with the abundance of carotenoids and polyphenols present in peach-derived products, which are enriched in fresh-fruit-derived preparations (Peel and FPP) but are also present in PPP. The Syrup - which was the least enriched in antioxidants - displayed no protective effect in our experiments. These effects cumulated in decreased levels of transaminases and lactate dehydrogenase leakage into serum and maintenance of organ architecture. Therefore, the herein presented results show evidence that supplementation with peach products may be protective against organ damage caused by oxidative stress, being interesting candidates for production of antioxidant-enriched functional foods.

Protective Effects of Lemon Juice on Alcohol-Induced Liver Injury in Mice

“…Therefore, lemon juice decreased the activities of SOD and CAT. The results were similar to the report of Gasparotto et al [22]. In addition, the in vitro antioxidant experiment of lemon also showed that lemon had medium in vitro antioxidant capacities, which contribute to the explanation of the in vivo free radical scavenging effect of lemon.…”

Targeting Reactive Carbonyl Species with Natural Sequestering Agents

“…Zucker rats [27] and ApoE null mice [28] have been employed to evaluate the reactive carbonyl species sequestering actions of carnosine and its derivatives, respectively. In addition, streptozotocin induced diabetic rats [29], CCl 4 -injected [30] or high fructose-fed [31] Wistar rats, and methylglyoxal injected Dahl salt-sensitive rats [32] were used to target reactive carbonyl species, AGEs, RAGE and/or protein carbonyls in diabetic complications. Furthermore, in humans, type II diabetic patients were studied for their elevated methyl glyoxal levels [19] as well as RAGE expression [33].…”

Effects of infliximab against carbon tetrachloride-induced intestinal injury via lipid peroxidation and apoptosis

“…10 MDA is a product of lipid peroxidation, and superoxide dismutase (SOD) is a scavenger enzyme of superoxide, and both are employed as indirect indicators of tissue damage. [11][12][13] This may indicate a different tissue damage mechanism of CCL 4 in intestinal tissue, or may perhaps be attributed to low study population numbers. 1,4,7,13,14 Administration of CCL 4 also stimulates the caspase pathway and regulates apoptosis.…”

“…4,9,13,[20][21][22][23] Such studies have shown that CCL 4 causes oxidative stress in a variety of organs and exhibits a broad range of toxicity. 12,13,17,23 Its toxic effects are due to its metabolites trichloromethyl free radical and trichloromethyl peroxyl radical, and also trigger the release of tumor necrosis factor-alpha (TNF-a) and interleukin-1 beta. 8,12,15,22 CCL 4 also induces tissue injury by enhancing lipid peroxidation, increasing MDA levels, and activating caspases.…”

“…12,13,17,23 Its toxic effects are due to its metabolites trichloromethyl free radical and trichloromethyl peroxyl radical, and also trigger the release of tumor necrosis factor-alpha (TNF-a) and interleukin-1 beta. 8,12,15,22 CCL 4 also induces tissue injury by enhancing lipid peroxidation, increasing MDA levels, and activating caspases. 13,17 8-Hydroxy-2 0 -deoxyguanosine (8-OHdG) has been used in a biomarker for the measurement of endogenous oxidative DNA damage.…”