Protective effect of apricot (Prunus armeniaca L.) on hepatic steatosis and damage induced by carbon tetrachloride in Wistar rats.

The present study was planned to investigate the protective effect of 10 % and 20 % apricot-containing feed on carbon tetrachloride (CCl4)-induced hepatic steatosis and damage. Adult male Wistar rats (n 42) were divided into six groups of seven each, as follows: control group; CCl4 group; CCl4+10 % apricot group; CCl4+20 % apricot group; 10 % apricot group; 20 % apricot group. All apricot groups were fed with 10 % or 20 % apricot-containing feed for 5 months. CCl4 injections were applied to the CCl4 groups at the dose of 1 mg/kg for 3 d at the end of 5 months. In the CCl4 group, vacuolated hepatocytes and hepatic necrosis were seen, especially in the centrilobular area. Hepatocytes showed an oedematous cytoplasmic matrix, large lipid globules and degenerated organelles. The area of liver injury was found significantly decreased with apricot feeding. Malondialdehyde and total glutathione levels and catalase, superoxide dismutase and glutathione peroxidase activities were significantly changed in the CCl4 group and indicated increased oxidative stress. Apricot feeding decreased this oxidative stress and ameliorated histological damage. We concluded that apricot feeding had beneficial effects on CCl4-induced liver steatosis and damage probably due to its antioxidant nutrient (beta-carotene and vitamin) contents and high radical-scavenging capacity. Dietary intake of apricot can reduce the risk of liver steatosis and damage caused by free radicals.

Beneficial effects of apricot-feeding on myocardial ischemia-reperfusion injury in rats.

The present study was undertaken to evaluate the cardio-protective potential of apricot-feeding in the ischemia-reperfusion (I/R) model of rats in vivo. Rats were divided into three groups of 12 rats each. Group 1 was fed with a standard rat chow, groups 2 and 3 were fed with a standard rat chow supplemented with 10% or 20% dried apricot during 3 months before the beginning of I/R studies. To produce I/R, the left main coronary artery was occluded for 30 min, followed by 120 min reperfusion, in anesthetized rats. Infarct sizes were found significantly decreased in 10% (55.0 +/- 4.3%) and 20% (57.0 +/- 2.9%) apricot-fed groups compared to control group (68.7 +/- 2.0%). Light and electron microscopic evaluations of hearts also demonstrated similar beneficial effects on I/R injury in apricot-fed both groups. Total phenolic contents, DPPH radical scavenging and ferric-reducing power as in vitro antioxidant capacities of rat chows were significantly increased after supplementation with apricot for each ratio. Cu, Zn Superoxide dismutase (Cu, Zn SOD) and catalase (CAT) activities were increased, and lipid peroxidation was decreased significantly in the hearts of 20% apricot-fed group after I/R. In conclusion, we clearly demonstrated in vivo cardio-protective activity of apricot-feeding related to its antioxidant phenolic contents in rats subjected to myocardial I/R.

Potent protective effect of apricot and beta-carotene on methotrexate-induced intestinal oxidative damage in rats.

Several studies have well confirmed the contribution of oxidative stress in the pathogenesis of methotrexate (MTX)-induced damage in the small intestine. Many agents have been tried experimentally to reduce or inhibit the oxidative stress. To our knowledge, there is no study about apricot consumption on the MTX-induced damage in the small intestine. The aim of this study was to determine the possible protective effects of apricot and beta-carotene on MTX-induced intestinal damage in rats. The rats were randomly divided into seven groups as follows; I-control group; II-apricot group; III-beta-carotene group; IV-MTX group; V-apricot+MTX group; VI-beta-carotene+MTX group and VII-apricot+beta-carotene+MTX group. In the MTX group; fusion and shortening in the villus, epithelial desquamation, crypt loss, inflammatory cell infiltration in the lamina propria, goblet cell depletion and microvillar damage were observed in the small intestine. Parallel to histological results, malondialdehyde (MDA) content and myeloperoxidase (MPO) activity were found to be increased, whereas superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GP-x) activities and glutathione (GSH) content were decreased in the MTX group. However, single or combined application of apricot and beta-carotene ameliorated all of these hazardous effects in antioxidant system in MTX-treated groups. In conclusion, our results demonstrate that apricot and/or beta-carotene treatment may protect the impairment of oxidative stress and ameliorate MTX-induced intestine damage at biochemical and histological levels.

The effect of melatonin on 7,12-dimethyl-benz[a]anthracene injury in comparison with vitamin E + selenium in mouse kidneys.

The aims of this study were to observe the changes in antioxidative defense enzymes and renal morphology after 7,12-dimethyl-benz[a]anthracene (7,12-DMBA) administration in mice and to investigate the possible protective effects of melatonin against 7,12-DMBA-induced renal damage in comparison with vitamin E + selenium (vit E + Se). Forty female mice were divided into four groups: control, DMBA, DMBA + vit E + Se and DMBA + melatonin. In the DMBA group, mice were given injections of 7,12-DMBA (20 mg/kg). DMBA + vit E + Se group mice received injections of 7,12-DMBA + vit E + Se (20 mg/kg + 90 mg/kg + 1.8 microg/kg). In the melatonin group, mice were given injections of 7,12-DMBA + melatonin (20 mg/kg + 4.2 mg/kg). The experiment lasted for 21 days. Mice were killed and the kidneys were taken for enzyme analyses and histologic examination. Catalase (CAT) and glutathione peroxidase (GSH-Px) activities were found significantly decreased in the DMBA group and in the DMBA + vit E + Se group when compared with the control group (P < 0.05), whereas CAT and GSH-Px activities were found significantly elevated in the DMBA + melatonin group when compared with the control (P < 0.05) and the DMBA group (P < 0.01). Exposure to DMBA resulted in tubular alterations in renal cortex. Morphometric analysis revealed proximal and distal tubular damage (P < 0.05). These alterations were found to be prevented by melatonin but not with vit E + Se administration. These results reveal that melatonin stimulates CAT and GSH-Px activities and prevents renal injury better than vit E + Se combination in mice kidneys.

Protective effect of oral L-arginine supplementation on cyclosporine induced nephropathy in rats.

BACKGROUND: One of the major adverse effects of long term cyclosporine A (CyA) administration is chronic nephrotoxicity. Several studies have suggested that alterations of the L-arginine (L-Arg) nitric oxide (NO) pathway may be involved in the pathogenesis of CyA-induced kidney damage. AIM: We postulated that in vivo activation of L-Arg-NO pathway might have a beneficial effect on CyA-induced renal damage. Conditions of chronic NO enhancement was established with L-Arg supplementation and chronic NO blockade with N-nitro-L-Arg methyl ester (L-NAME). We tested the hypothesis that, if CyA administration alters intrarenal NO synthesis, then exogenous L-Arg supplementation could limit renal injury, on the contrary, L-NAME, a potent competitive inhibitor of NO synthesis, could enhance CyA nephrotoxicity. Harmful effect of NO blockade indirectly supports the beneficial effect of NO in a model of CyA nephrotoxicity. METHODS: Rats were administered vehicle (VH), CyA (7.5 mg/kg/day), CyA + L-Arg (2g/kg/day), CyA + L-NAME (5 mg/100 ml/day), CyA + L-Arg + L-NAME, VH + L-Arg, VH + L-NAME and were sacrificed at the end of the experiment. Body weight, serum creatinine, blood urea nitrogen (BUN) and NO levels were determined. Tubular injury and interstitial fibrosis were evaluated semiquantitatively using scoring systems on paraffin sections stained with hematoxylin/eosin (H/E), Masson's trichromic and periodic acid-Schiff (PAS). RESULTS: The CyA group developed marked renal injury, characterized by a significant increase in serum creatinine and BUN, and histopathological alterations including tubular dilatation, vacuolization, necrosis, interstitial cell infiltration and tubulointerstitial fibrosis. CyA reduced serum NO level. L-Arg treatment significantly enhanced NO biosynthesis and protected animals from CyA-induced kidney damage. In contrast L-NAME strikingly reduced serum NO level, and worsened biochemical and histopathological alterations. CONCLUSION: Chronic CyA nephrotoxicity can be aggravated by NO blockade and ameliorated by NO enhancement suggesting that L-Arg supplementation may be protective in CyA nephrotoxicity.

Comparison of chemopreventive effects of Vitamin E plus selenium versus melatonin in 7,12-dimethylbenz(a)anthracene-induced mouse brain damage.

In this work, the protective effect of Vitamin E plus selenium (Vit E+Se) and melatonin against 7,12-dimethylbenz(a)anthracene (7,12-DMBA)-induced changes in superoxide dismutase (SOD), glutathione peroxidase (GSHPx), catalase (CAT) and carbonic anhydrase (CA) activities and malonedialdehyde (MDA) levels of mouse brain were compared. 12-month old mice were divided into four groups each including 10 animals. The first group served as control group. The second group was treated with 7,12-DMBA (20 mg/(kg day)). The third group was treated with 7,12-DMBA and Vitamin E (90 microg/(individual day)) and selenium (1.8 microg/(individual day)) simultaneously. The fourth group was treated with 7,12-DMBA and melatonin (4.2 mg/(kg day)) simultaneously. Treatment continued for 21 days after which the mice were sacrificed and brain homogenates were prepared. 7,12-DMBA treated group exhibited significantly decreased levels of brain SOD, GSHPx, CAT and CA activities and increased MDA levels as compared to control. Vitamin E+Se fully or partially restored enzyme inhibition except for SOD. Lipid peroxidation was also reduced in Vitamin E+Se treated group. Melatonin provided a better protection for SOD, GSHPx and CAT, and a plausible protection for CA activity. Protection against lipid peroxidation measured as MDA in melatonin treated group was appreciable although slightly lesser than the protection provided by Vitamin E+Se. The results imply that Vitamin E+Se and melatonin both provide chemoprevention against 7,12-DMBA-induced oxidative stress in mouse brain.