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Caffeic acid phenethyl ester (CAPE) ameliorates cisplatin-induced hepatotoxicity in rabbit

In this study, it was aimed to investigate the protective effect of caffeic acid phenethyl ester (CAPE) on cisplatin hepatotoxicity. Thirty New Zealand rabbits were divided into 5 groups as group 1 (saline-injected control, C), group 2 (1% ethanol; vehicle for CAPE, E), group 3 (CAPE), group 4 (cisplatin, CS) and group 5 (cisplatin plus CAPE, CS+CAPE). Cisplatin caused increased immunoreactivity against inducible nitric oxide synthase (iNOS), but CAPE treatment reduced the immunoreactive hepatocytes. Liver malondialdehide (MDA), nitric oxide (NO(.)) levels and xanthine oxidase (XO) activities were higher in CS than in groups C and E. Cisplatin treatment also significantly decreased the tissue reduced glutathione (GSH) concentration compared to groups C and E. CAPE administration normalized the tissue GSH level and XO activity in group CS+CAPE, whereas CAPE treatment did not affect MDA level in group CS+CAPE. In addition, CAPE treatment significantly depressed the cisplatin-induced NO(.) increase in group CS+CAPE. Histopathologically, cisplatin caused hydropic degenerations, necrosis in hepatocytes, sinusoidal congestion, Kupffer cell proliferation and mononuclear cell infiltration. These alterations were less severe in rabbits receiving CS+CAPE. Parallel to histopathology, cisplatin increased serum AST and ALT levels, whereas CAPE treatment significantly reduced cisplatin-induced AST and ALT rise in the serum. Results suggest that cisplatin causes oxidative and nitrosative damage to hepatocytes. Cisplatin-induced increase in XO and NO(.) could contribute oxidative stress in the hepatotoxicity. CAPE shows partial protection against cisplatin-associated biochemical and histopathological alterations.

The effects of chronic exposure to ethanol and cigarette smoke on the formation of peroxynitrite, level of nitric oxide, xanthine oxidase and myeloperoxidase activities in rat kidney

The aim of this study was to investigate the effects of chronic ethanol intake and cigarette smoke exposure on rat kidney. The animals were divided into four experimental groups: (1) the control group (C), (2) the ethanol group (E), (3) the cigarette smoke group (CS), and (4) the cigarette smoke plus ethanol group (CS+E). Rats in E, CS and CS+E groups were treated with ethanol and/or cigarette smoke for 6 months. The animals were killed and the kidneys were removed to determine the activity of xanthine oxidase (XO), myeloperoxidase (MPO) and the levels of nitric oxide (NO). Histopathological and immunohistochemical analysis were performed in kidney tissues. The activity of XO/g protein were 2.8 ± 0.3, 5.2 ± 0.3, 3.2 ± 0.1, and 7.4 ± 0.7 U for C, E, CS and CS+E groups, respectively. In groups E, and CS+E, the XO values were significantly higher than in group C (P < 0.05). The increase in XO activity of CS was not significantly different from group C (P > 0.05). There was a significant increase in XO activity of group CS+E as compared to CS and E groups (P < 0.05), and also a significant difference in XO activity between E and CS was observed (P < 0.05). The activity of MPO/g protein were 13.5 ± 0.6, 16.2 ± 1.1, 14.7 ± 1.1, 23.8 ± 0.9 U for C, E, CS, and CS+E groups, respectively. While MPO activity of kidneys from group CS+E were significantly higher as compared to C, CS, and E groups (P < 0.05), there was no significant difference among the groups of C, CS, E (P > 0.05). The levels of NO/g wet tissue were 347.7 ± 8.5, 261.1 ± 4.8, 329.8 ± 5.6, and 254.2 ± 3.8 nmol for C, E, CS, and CS+E groups, respectively. In groups of E and CS+E, the NO values were significantly lower than that of group C animals (P < 0.05). Although we detected lower NO levels in the E and CS+E groups than in CS group (P < 0.05), a significant difference in NO levels between CS+E and E groups was not observed. In the histopathological analysis of the kidney slices, severe degenerations in kidney tissues of group CS, E, CS+E were observed. Generally, the histological changes in kidney of CS+E and E groups were more severe than those observed in CS alone. While we observed a strong immunoreactivity for anti-nitrotyrosine antibody in kidneys of group CS+E, examination of sections from rat kidneys in group E revealed moderate staining. On the other hand, group CS had very little immunostaining. There was no immunostaining in group C.We concluded that chronic ethanol administration and cigarette smoke exposure may cause oxidative and nitrosative stress which lead to rat kidney damage.

Resveratrol ameliorates cisplatin-induced oxidative injury in New Zealand rabbits

This study investigated the preventive role of resveratrol in cisplatin-induced nephrotoxicity. The study used groups of New Zealand rabbits that were treated as follows: group C (cisplatin treated), group R (resveratrol treated), group R+C (resveratrol + cisplatin treatment), and group E (control group). Kidney levels of glutathione were significantly lower in group C than in groups E and R, whereas glutathione levels in group R+C were found to be similar to the control values. Malondialdehyde levels in group C were significantly higher than in groups E and R. However, malondialdehyde levels in group R+C were similar to group E. Kidney levels of nitric oxide were significantly higher in the cisplatin group than in the control, whereas nitric oxide levels were at basal values in group R+C. Cisplatin treatment significantly reduced kidney levels of glutathione peroxidase, superoxide dismutase, and catalase activity compared with those of group E, whereas resveratrol treatment significantly increased levels of glutathione peroxidase, superoxide dismutase, and catalase activity in group R+C. However, cisplatin injection did not affect mRNA levels of glutathione peroxidase, superoxide dismutase, or catalase enzymes. Histopathological and immunohistochemical analyses indicated that cisplatin caused kidney damage, which was mostly prevented by resveratrol treatment. In conclusion, resveratrol ameliorates cisplatin-induced oxidative injury in the kidney of rabbit.

Attenuation of ischemia–reperfusion injury with Marrubium cordatum treatment in ovarian torsion–detorsion model in rabbits

OBJECTIVE To investigate protective effects of Marrubium cordatum extract on ovary torsion-detorsion. DESIGN Controlled research study. SETTING Marrubium cordatum extract was obtained by methanol extraction. ANIMAL(S) Six-month-old female New Zealand rabbits. INTERVENTION(S) In the first phase, antioxidant activity of M. cordatum extract was evaluated. In the second phase, M. cordatum extract at doses of 0, 250, 500, and 1,000 mg/kg was studied for dose determination. In the third phase, the protective role of M. cordatum on ovarian torsion-detorsion injury was evaluated in sham control, torsion-detorsion, torsion-detorsion +M. cordatum (1,000 mg/kg). MAIN OUTCOME MEASURE(S) 1,1-Diphenyl-2-picrylhydrazyl, nitric oxide radical scavenging activity, reducing power capacity, and total phenolic compounds were assayed. Glutathione, malondialdehyde, catalase, and glutathione peroxidase were measured. Histopathological examination was also conducted. RESULT(S) Marrubium cordatum significantly inhibited 1,1-diphenyl-2-picrylhydrazyl, nitric oxide radicals, and showed a powerful reducing activity. Marrubium cordatum did not adversely affect biochemical and histopathological parameters at all doses. Malondialdehyde level and catalase activity in the torsion-detorsion group were significantly increased compared with those of the sham group, whereas the glutathione level and glutathione peroxidase activity were significantly decreased compared with those of the sham group. Marrubium cordatum treatment significantly lowered the malondialdehyde level and catalase activity but increased the glutathione level in torsion-detorsion injury. Histopathologically, severe congestion, hemorrhage, edema, and leukocyte infiltration were observed in the torsion-detorsion group. Marrubium cordatum treatment ameliorated these alterations. CONCLUSION(S) Marrubium cordatum attenuates ischemia-reperfusion-induced biochemical and histopathological alterations.

Effects of organophosphate phenyl saligenin phosphate and polyether carboxylic ionophore lasalocid on motor nerve conduction velocity, neuropathy target esterase enzyme activity, and clinical ataxia in chickens

Organophosphates (OP) are widely used chemicals in agriculture and industry. Some OPs produce a delayed type of neuropathy affecting human and animals following exposure. Subacute neurotoxic doses of some OPs can be potentiated by concomitant exposure to certain chemicals. Lasalocid is a polyether carboxylic ionophore used as a growth promotant and anti-coccidial in the cattle and poultry industries, respectively. Lasalocid is also known to induce peripheral neuropathy. Neurotoxicity of phenyl saligenin phosphate (PSP) and lasalocid and possible interaction were studied in chickens by evaluating motor nerve conduction velocity (MNCV), clinical ataxia, and neuropathy target esterase (NTE) enzyme activity. Forty-eight fryer chickens were divided into four groups as follows: Group 1 (control), group 2 was injected with single subcutaneous (s.c.) PSP (5 mg/kg), group 3 received oral lasalocid sodium (20 mg/kg, b.i.d., for 2 days), and group 4 received single s.c. PSP injection plus oral lasalocid sodium. MNCVs were decreased in groups 2, 3, and 4 compared to control. While there was no difference in MNCV between groups 2 and 3 (p > 0.05), MNCV in group 4 were significantly lower than in groups 2 and 3 (p < 0.05). NTE activities were significantly lower in PSP and PSP+lasalocid groups than in control and lasalocid group (p < 0.05). Onset of ataxia in group 4 appeared early and was exacerbated compared to groups 2 and 3. In conclusion, PSP and lasalocid could induce a significant decrease in MNCV and produce ataxia. Neuropathic OPs could be exacerbated by polyether ionophore lasalocid.