Abstract: The objective of this study was to compare the beneficial effects of caffeic acid phe... more Abstract: The objective of this study was to compare the beneficial effects of caffeic acid phenethyl ester (CAPE), vitamin C, vitamin E and N-acetylcysteine on vancomycin-induced nephrotoxicity. Thirty rats were randomly devided into six groups: (i) control; (ii) vancomycin, 200 mg/kg administrated via intraperitoneal route; (iii) vancomycin plus CAPE – vancomycin with 10 µmol/kg CAPE; (iv) vancomycin plus vitamin C – vancomycin (intraperitoneally) with 200 mg/dl vitamin C in drinking water; (v) vancomycin plus vitamin E – vancomycin with 1000 mg/kg body weight vitamin E (intramuscularly); and (vi) vancomycin plus N-acetylcysteine – vancomycin with 10 mg/kg body weight (intraperitoneally) of N-acetylcysteine. Vancomycin treatments were started 1 day after the first administrations of these agents and continued for 7 days. At the end of the experiments, catalase activity was significantly decreased by vancomycin in kidney homogenates (P < 0.05). Vitamin E, vitamin C, N-acetylcysteine and CAPE administrations decreased the blood urea nitrogen levels increased by vancomycin, although significant differences were detected only in the vitamins E and C groups (P < 0.05). Increased renal malondialdehyde and nitric oxide levels by vancomycin were significantly suppressed by agents used in the study (P < 0.05). Histopathological examination demonstrated prominent damages in the vancomycin-treated group. Vitamin E was the most beneficial agent on vancomycin-induced tubular damage, followed by vitamin C, N-acetylcysteine and CAPE treatments, respectively. The data suggest that vitamin E, as well as vitamin C, N-acetylcysteine and CAPE, could be useful for reducing the detrimental effects on vancomycin-induced toxicity in kidneys.
Cadmium (Cd) exposure has been recognized to result in a wide variety of cellular responses, incl... more Cadmium (Cd) exposure has been recognized to result in a wide variety of cellular responses, including oxidative stress and body weight loss. The aim of the present study was to examine the effect of lycopene supplementation on the antioxidant defense system, lipid peroxidation (LPO) level, nitric oxide (NO), tumor necrosis factor alpha (TNF-α) production, and body weight in Cd-exposed rats. Animals were divided into four groups (n = 7): control, Cd-treated, Cd plus lycopene-treated, and lycopene-treated. Cadmium (as CdCl2) was administrated orally for 20 days (6.6 mg kg−1 day−1), and lycopene (10 mg kg−1 day−1) was similarly administered. Lycopene administration significantly suppressed Cd-induced LPO in plasma and kidney homogenates. Lycopene also reversed Cd-decreased body weight compared to the control. Cadmium treatment had diverse effects on the antioxidant enzyme activities. Although antioxidant superoxide dismutase activity was unchanged, glutathione peroxidase activity was decreased, and catalase activity was elevated in kidney homogenates of Cd-administrated group. However, lycopene treatment reversed Cd-changed enzyme activities to the control level. Xanthine oxidase activity and TNF-α concentration were not altered by Cd administration, indicating that superoxide anion production and inflammation were not stimulated. Cadmium did not change NO levels in kidney homogenates but decreased those in plasma, and this effect was not prevented by lycopene supplementation. The result suggests that consumption of adequate levels of lycopene may be useful to prevent heavy-metal-induced LPO and body weight loss.
The objective of this study was to collect rectal swabs from the cattle in a slaughterhouse locat... more The objective of this study was to collect rectal swabs from the cattle in a slaughterhouse located in Hatay (Turkey) immediately after slaughter for the isolation and characterization of verotoxin-producing Escherichia coli O157 in each month during a 1-year period. The rectal swab samples were analyzed for the isolation of E. coli O157 through preenrichment, immunomagnetic separation and selective plating on CT-SMAC agar. E. coli O157 was isolated from 77 (13.6%) of the samples. The presence of E. coli O157 changed during a 1-year period, in that the occurrence of E. coli O157 was the highest in July and November and lowest in February. A total of 66 isolates out of 77 were seroytpe O157:H7 and 11 were serotype O157:NM. PCR analysis of E. coli O157 virulence genes revealed that all O157:H7/NM were positive for rbfO157, 74 positive for EhlyA, 72 positive for eaeA, 62 positive for vtx2, and 3 positive for both vtx1 and vtx2. It was presented by cytotoxicity tests that many of E. coli O157 isolates showed high cytotoxicity on Vero cells. All of the isolates containing EhlyA showed enterohaemolysin production.
Journal of Veterinary Medicine Series A-physiology Pathology Clinical Medicine, 2003
A total of 135 laying quails (Coturnix coturnix japonica), 9 weeks old, were divided into three d... more A total of 135 laying quails (Coturnix coturnix japonica), 9 weeks old, were divided into three dietary treatment groups. Three replicates were assigned to each treatment group consisting of 15 birds per cage. The diet was supplemented with 0, 100 and 200 ppm Yucca schidigera powder and given ad libitum to the quails for a period of 14 weeks. Body weight, egg production, feed consumption and feed efficiency were not different due to dietary treatments among the groups. Increased egg weight was determined in the control group.Yucca powder supplementation decreased serum glucose, cholesterol and triglyceride level in laying quails. Serum total protein concentration was not changed by dietary treatments but albumin level was decreased in quails fed 100 ppm yucca powder. Egg yolk cholesterol concentration was not significantly different among the groups but tended to decline (11.5%) as a result of yucca supplementation. Red Blood Cell (RBC) and White Blood Cell (WBC) counts, packed cell volume (PCV), mean corpuscular volume (MCV) and mean corpuscular haemoglobin (MCH) were not affected by supplementation of yucca powder. However, haemoglobin (HB) concentration was slightly increased and mean corpuscular haemoglobin concentration (MCHC) was significantly increased by 200 ppm yucca powder supplementation to the diet.
Caffeic acid phenethyl ester (CAPE) was screened for hypoglycemic and liver-protective activity i... more Caffeic acid phenethyl ester (CAPE) was screened for hypoglycemic and liver-protective activity in streptozotocin (STZ)-induced diabetic rats. Diabetes was established by single dose STZ injection (45 mg kg−1 bw, i.p.) for 48 h. CAPE was injected at doses of 10, 20 and 30 μM kg−1 bw day−1 (i.p.) to the rats in CAPEI, CAPEII and CAPEIII groups 2 days after induction of diabetes and continued for 60 days, thereafter. It was found that diabetes down-regulated the expressions of glucokinase (7.8-fold) and pyruvate kinase (6.4-fold) in comparison to control, however, phoshoenolpyruvate carboxykinase mRNA levels were up-regulated by 2.2-fold. CAPE treatments enhanced the expressions of glucokinase (3.4–14.9-folds), and pyruvate kinase (3.2–12.8-folds) mRNAs in diabetic rats. However, phoshoenolpyruvate carboxykinase mRNA expression was decreased by CAPE to varying degrees (1.2–5.5-fold). CAPE increased (∼2-fold) the level of plasma insulin previously decreased by STZ treatment. Here we demonstrate that CAPE significantly decreased the fasting blood levels of glucose, alanine aminotransferase, cholesterol, and triglyceride induced by diabetes. CAPE increased the liver glycogen level lowered by diabetes. In histopathological evaluation of the liver, CAPE treatments were seen to reduce necrosis and anisonucleosis in hepatocytes, and connective tissue elevated in the portal region by diabetes. CAPE exhibits a significant potential as an antidiabetic agent by suppressing hepatic glucose output via inducing mRNA expression of glucokinase and pyruvate kinase, whilst inhibiting phoshoenolpyruvate carboxykinase in diabetes. CAPE also has the ability to decrease the harmful effects of diabetes on the liver of rats.
Journal of Animal Physiology and Animal Nutrition, 2010
The current study was conducted to evaluate the effects of dietary supplementation of synbiotics ... more The current study was conducted to evaluate the effects of dietary supplementation of synbiotics and phytobiotics on performance, small intestine weight, pH and caecal coliform counts of broilers. The influences of synbiotics and phytobiotics on oxidant/antioxidant status in the blood of broilers were also assessed. A total of 200 broiler chicks were randomly allotted to four dietary treatments, either fed a basal diet or the same diet supplemented with 1 g/kg synbiotic, 1 g/kg phytobiotic or 1 g/kg synbiotic plus 1 g/kg phytobiotic. The diet supplemented with both synbiotic and phytobiotic had no effect on body weight, body weight gain, feed intake and feed efficiency of broilers at the end of the study (p > 0.05). Neither small intestine weight nor pH was affected by any of the treatments. Supplementation of both synbiotic and phytobiotic to diet decreased the caecal coliform count (p < 0.01). Addition of synbiotics and phytobiotics in combination significantly increased plasma malondialdehyde (MDA) levels (p ≤ 0.05), whereasphytobiotic addition alone showed only a slight increase. Similarly, elevated nitric oxide (NO) level was recorded in the synbiotic- and phytobiotic-fed group and in the phytobiotic-fed group (p ≤ 0.001). Superoxide dismutase (SOD) activities did not differ between the groups. In conclusion, dietary supplementation of synbiotic and phytobiotic improved the gut health by decreasing the caecal total coliform count, but growth performance was not affected by the supplementations. Further investigations are needed to determine the effects of phytobiotics on oxidative/antioxidative metabolism as regards their compositional analysis.
Although oxidative damage is known to be involved in inflammatory-mediated tissue destruction, mo... more Although oxidative damage is known to be involved in inflammatory-mediated tissue destruction, modulation of oxygen free radical production represents a new approach to the treatment of inflammatory diseases. Caffeic acid phenethyl ester (CAPE), an active component of propolis from honeybee hives, has antioxidant, anti-inflammatory and antibacterial properties. For that reason, we aimed to investigate the efficiency of CAPE administration in preventing oxidative damage in pyelonephritis (PYN) caused by Escherichia coli. In this study, 35 Wistar rats were grouped as follows: control, PYN 24 h, PYN 48 h, PYN 72 h, CAPE 24 h, CAPE 48 h and CAPE 72 h. E. coli (1 × 109 c.f.u.) were inoculated into the rats in both PYN and CAPE groups via urethral catheterization. Ten μM/kg-body weight CAPE was injected to the rats in all CAPE groups 24 h before E. coli infection, and injections were repeated at 24-h intervals. Rats were sacrificed 24 h, 48 h and 72 h after infection in both PYN and CAPE groups. Malondialdehyde (MDA) and nitric oxide (NO) levels were significantly increased in kidneys of PYN groups. The activities of the antioxidant enzymes, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and xanthine oxidase (XO) were also elevated by E. coli. However, CAPE administration reduced MDA and NO levels, as well as XO activity, although it increased SOD and GSH-Px activities. Histopathological examination showed that CAPE reduced the inflammation grade induced by E. coli. In conclusion, CAPE administrations decrease the oxidative damage occurring in PYN and therefore could be used for medical management of bacterial nephropathy.
Pesticide Biochemistry and Physiology - PESTIC BIOCHEM PHYSIOL, 2010
Imidacloprid is a neonicotinoid insecticide and has been extensively used as a crop pest and pet ... more Imidacloprid is a neonicotinoid insecticide and has been extensively used as a crop pest and pet flea control programme because it’s high specificity as an insecticide. Imidacloprid toxicity on mammalian tissues has not been adequately evaluated. In the present study, potential acute neuro and liver toxic effects of imidacloprid were analyzed in rats as a model of mammalian using antioxidant–oxidant and inflammatory system. 10 μM imidacloprid was administrated intravenously and 2 h post-administration, the rats were sacrificed, liver and brains were surgically removed. Exposure to imidacloprid led to significant increases in nitric oxide concentrations in brain, liver and plasma samples. The quantitative mRNA transcriptional analyses demonstrated that imidacloprid-elevated production of NO levels due to the induction of iNOS in liver, but neither nNOS nor iNOS were induced in brain. The oxidant-generating enzymes xanthine oxidase and myeloperoxidase activities in both tissues were elevated and significant lipid peroxidation in liver and plasma was observed. The antioxidant catalase, superoxide dismutase and glutathione peroxidase activities were differently responded to imidacloprid administration. Significant intracellular glutathione depletion was also measured in both tissues. Imidacloprid treatment up-regulated inflammatory cytokines TNF-α, IL-6 and IL-1β mRNA transcriptions by 2.5- to 5.2-fold increases in both brain and liver. Conversely, anti-inflammatory mediator IL-10 mRNA was down-regulated in both organs. These results suggest that imidacloprid cause oxidative stress and inflammation in central nervous system and liver in non-target organisms in rats.
Abstract: The objective of this study was to compare the beneficial effects of caffeic acid phe... more Abstract: The objective of this study was to compare the beneficial effects of caffeic acid phenethyl ester (CAPE), vitamin C, vitamin E and N-acetylcysteine on vancomycin-induced nephrotoxicity. Thirty rats were randomly devided into six groups: (i) control; (ii) vancomycin, 200 mg/kg administrated via intraperitoneal route; (iii) vancomycin plus CAPE – vancomycin with 10 µmol/kg CAPE; (iv) vancomycin plus vitamin C – vancomycin (intraperitoneally) with 200 mg/dl vitamin C in drinking water; (v) vancomycin plus vitamin E – vancomycin with 1000 mg/kg body weight vitamin E (intramuscularly); and (vi) vancomycin plus N-acetylcysteine – vancomycin with 10 mg/kg body weight (intraperitoneally) of N-acetylcysteine. Vancomycin treatments were started 1 day after the first administrations of these agents and continued for 7 days. At the end of the experiments, catalase activity was significantly decreased by vancomycin in kidney homogenates (P < 0.05). Vitamin E, vitamin C, N-acetylcysteine and CAPE administrations decreased the blood urea nitrogen levels increased by vancomycin, although significant differences were detected only in the vitamins E and C groups (P < 0.05). Increased renal malondialdehyde and nitric oxide levels by vancomycin were significantly suppressed by agents used in the study (P < 0.05). Histopathological examination demonstrated prominent damages in the vancomycin-treated group. Vitamin E was the most beneficial agent on vancomycin-induced tubular damage, followed by vitamin C, N-acetylcysteine and CAPE treatments, respectively. The data suggest that vitamin E, as well as vitamin C, N-acetylcysteine and CAPE, could be useful for reducing the detrimental effects on vancomycin-induced toxicity in kidneys.
Cadmium (Cd) exposure has been recognized to result in a wide variety of cellular responses, incl... more Cadmium (Cd) exposure has been recognized to result in a wide variety of cellular responses, including oxidative stress and body weight loss. The aim of the present study was to examine the effect of lycopene supplementation on the antioxidant defense system, lipid peroxidation (LPO) level, nitric oxide (NO), tumor necrosis factor alpha (TNF-α) production, and body weight in Cd-exposed rats. Animals were divided into four groups (n = 7): control, Cd-treated, Cd plus lycopene-treated, and lycopene-treated. Cadmium (as CdCl2) was administrated orally for 20 days (6.6 mg kg−1 day−1), and lycopene (10 mg kg−1 day−1) was similarly administered. Lycopene administration significantly suppressed Cd-induced LPO in plasma and kidney homogenates. Lycopene also reversed Cd-decreased body weight compared to the control. Cadmium treatment had diverse effects on the antioxidant enzyme activities. Although antioxidant superoxide dismutase activity was unchanged, glutathione peroxidase activity was decreased, and catalase activity was elevated in kidney homogenates of Cd-administrated group. However, lycopene treatment reversed Cd-changed enzyme activities to the control level. Xanthine oxidase activity and TNF-α concentration were not altered by Cd administration, indicating that superoxide anion production and inflammation were not stimulated. Cadmium did not change NO levels in kidney homogenates but decreased those in plasma, and this effect was not prevented by lycopene supplementation. The result suggests that consumption of adequate levels of lycopene may be useful to prevent heavy-metal-induced LPO and body weight loss.
The objective of this study was to collect rectal swabs from the cattle in a slaughterhouse locat... more The objective of this study was to collect rectal swabs from the cattle in a slaughterhouse located in Hatay (Turkey) immediately after slaughter for the isolation and characterization of verotoxin-producing Escherichia coli O157 in each month during a 1-year period. The rectal swab samples were analyzed for the isolation of E. coli O157 through preenrichment, immunomagnetic separation and selective plating on CT-SMAC agar. E. coli O157 was isolated from 77 (13.6%) of the samples. The presence of E. coli O157 changed during a 1-year period, in that the occurrence of E. coli O157 was the highest in July and November and lowest in February. A total of 66 isolates out of 77 were seroytpe O157:H7 and 11 were serotype O157:NM. PCR analysis of E. coli O157 virulence genes revealed that all O157:H7/NM were positive for rbfO157, 74 positive for EhlyA, 72 positive for eaeA, 62 positive for vtx2, and 3 positive for both vtx1 and vtx2. It was presented by cytotoxicity tests that many of E. coli O157 isolates showed high cytotoxicity on Vero cells. All of the isolates containing EhlyA showed enterohaemolysin production.
Journal of Veterinary Medicine Series A-physiology Pathology Clinical Medicine, 2003
A total of 135 laying quails (Coturnix coturnix japonica), 9 weeks old, were divided into three d... more A total of 135 laying quails (Coturnix coturnix japonica), 9 weeks old, were divided into three dietary treatment groups. Three replicates were assigned to each treatment group consisting of 15 birds per cage. The diet was supplemented with 0, 100 and 200 ppm Yucca schidigera powder and given ad libitum to the quails for a period of 14 weeks. Body weight, egg production, feed consumption and feed efficiency were not different due to dietary treatments among the groups. Increased egg weight was determined in the control group.Yucca powder supplementation decreased serum glucose, cholesterol and triglyceride level in laying quails. Serum total protein concentration was not changed by dietary treatments but albumin level was decreased in quails fed 100 ppm yucca powder. Egg yolk cholesterol concentration was not significantly different among the groups but tended to decline (11.5%) as a result of yucca supplementation. Red Blood Cell (RBC) and White Blood Cell (WBC) counts, packed cell volume (PCV), mean corpuscular volume (MCV) and mean corpuscular haemoglobin (MCH) were not affected by supplementation of yucca powder. However, haemoglobin (HB) concentration was slightly increased and mean corpuscular haemoglobin concentration (MCHC) was significantly increased by 200 ppm yucca powder supplementation to the diet.
Caffeic acid phenethyl ester (CAPE) was screened for hypoglycemic and liver-protective activity i... more Caffeic acid phenethyl ester (CAPE) was screened for hypoglycemic and liver-protective activity in streptozotocin (STZ)-induced diabetic rats. Diabetes was established by single dose STZ injection (45 mg kg−1 bw, i.p.) for 48 h. CAPE was injected at doses of 10, 20 and 30 μM kg−1 bw day−1 (i.p.) to the rats in CAPEI, CAPEII and CAPEIII groups 2 days after induction of diabetes and continued for 60 days, thereafter. It was found that diabetes down-regulated the expressions of glucokinase (7.8-fold) and pyruvate kinase (6.4-fold) in comparison to control, however, phoshoenolpyruvate carboxykinase mRNA levels were up-regulated by 2.2-fold. CAPE treatments enhanced the expressions of glucokinase (3.4–14.9-folds), and pyruvate kinase (3.2–12.8-folds) mRNAs in diabetic rats. However, phoshoenolpyruvate carboxykinase mRNA expression was decreased by CAPE to varying degrees (1.2–5.5-fold). CAPE increased (∼2-fold) the level of plasma insulin previously decreased by STZ treatment. Here we demonstrate that CAPE significantly decreased the fasting blood levels of glucose, alanine aminotransferase, cholesterol, and triglyceride induced by diabetes. CAPE increased the liver glycogen level lowered by diabetes. In histopathological evaluation of the liver, CAPE treatments were seen to reduce necrosis and anisonucleosis in hepatocytes, and connective tissue elevated in the portal region by diabetes. CAPE exhibits a significant potential as an antidiabetic agent by suppressing hepatic glucose output via inducing mRNA expression of glucokinase and pyruvate kinase, whilst inhibiting phoshoenolpyruvate carboxykinase in diabetes. CAPE also has the ability to decrease the harmful effects of diabetes on the liver of rats.
Journal of Animal Physiology and Animal Nutrition, 2010
The current study was conducted to evaluate the effects of dietary supplementation of synbiotics ... more The current study was conducted to evaluate the effects of dietary supplementation of synbiotics and phytobiotics on performance, small intestine weight, pH and caecal coliform counts of broilers. The influences of synbiotics and phytobiotics on oxidant/antioxidant status in the blood of broilers were also assessed. A total of 200 broiler chicks were randomly allotted to four dietary treatments, either fed a basal diet or the same diet supplemented with 1 g/kg synbiotic, 1 g/kg phytobiotic or 1 g/kg synbiotic plus 1 g/kg phytobiotic. The diet supplemented with both synbiotic and phytobiotic had no effect on body weight, body weight gain, feed intake and feed efficiency of broilers at the end of the study (p > 0.05). Neither small intestine weight nor pH was affected by any of the treatments. Supplementation of both synbiotic and phytobiotic to diet decreased the caecal coliform count (p < 0.01). Addition of synbiotics and phytobiotics in combination significantly increased plasma malondialdehyde (MDA) levels (p ≤ 0.05), whereasphytobiotic addition alone showed only a slight increase. Similarly, elevated nitric oxide (NO) level was recorded in the synbiotic- and phytobiotic-fed group and in the phytobiotic-fed group (p ≤ 0.001). Superoxide dismutase (SOD) activities did not differ between the groups. In conclusion, dietary supplementation of synbiotic and phytobiotic improved the gut health by decreasing the caecal total coliform count, but growth performance was not affected by the supplementations. Further investigations are needed to determine the effects of phytobiotics on oxidative/antioxidative metabolism as regards their compositional analysis.
Although oxidative damage is known to be involved in inflammatory-mediated tissue destruction, mo... more Although oxidative damage is known to be involved in inflammatory-mediated tissue destruction, modulation of oxygen free radical production represents a new approach to the treatment of inflammatory diseases. Caffeic acid phenethyl ester (CAPE), an active component of propolis from honeybee hives, has antioxidant, anti-inflammatory and antibacterial properties. For that reason, we aimed to investigate the efficiency of CAPE administration in preventing oxidative damage in pyelonephritis (PYN) caused by Escherichia coli. In this study, 35 Wistar rats were grouped as follows: control, PYN 24 h, PYN 48 h, PYN 72 h, CAPE 24 h, CAPE 48 h and CAPE 72 h. E. coli (1 × 109 c.f.u.) were inoculated into the rats in both PYN and CAPE groups via urethral catheterization. Ten μM/kg-body weight CAPE was injected to the rats in all CAPE groups 24 h before E. coli infection, and injections were repeated at 24-h intervals. Rats were sacrificed 24 h, 48 h and 72 h after infection in both PYN and CAPE groups. Malondialdehyde (MDA) and nitric oxide (NO) levels were significantly increased in kidneys of PYN groups. The activities of the antioxidant enzymes, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and xanthine oxidase (XO) were also elevated by E. coli. However, CAPE administration reduced MDA and NO levels, as well as XO activity, although it increased SOD and GSH-Px activities. Histopathological examination showed that CAPE reduced the inflammation grade induced by E. coli. In conclusion, CAPE administrations decrease the oxidative damage occurring in PYN and therefore could be used for medical management of bacterial nephropathy.
Pesticide Biochemistry and Physiology - PESTIC BIOCHEM PHYSIOL, 2010
Imidacloprid is a neonicotinoid insecticide and has been extensively used as a crop pest and pet ... more Imidacloprid is a neonicotinoid insecticide and has been extensively used as a crop pest and pet flea control programme because it’s high specificity as an insecticide. Imidacloprid toxicity on mammalian tissues has not been adequately evaluated. In the present study, potential acute neuro and liver toxic effects of imidacloprid were analyzed in rats as a model of mammalian using antioxidant–oxidant and inflammatory system. 10 μM imidacloprid was administrated intravenously and 2 h post-administration, the rats were sacrificed, liver and brains were surgically removed. Exposure to imidacloprid led to significant increases in nitric oxide concentrations in brain, liver and plasma samples. The quantitative mRNA transcriptional analyses demonstrated that imidacloprid-elevated production of NO levels due to the induction of iNOS in liver, but neither nNOS nor iNOS were induced in brain. The oxidant-generating enzymes xanthine oxidase and myeloperoxidase activities in both tissues were elevated and significant lipid peroxidation in liver and plasma was observed. The antioxidant catalase, superoxide dismutase and glutathione peroxidase activities were differently responded to imidacloprid administration. Significant intracellular glutathione depletion was also measured in both tissues. Imidacloprid treatment up-regulated inflammatory cytokines TNF-α, IL-6 and IL-1β mRNA transcriptions by 2.5- to 5.2-fold increases in both brain and liver. Conversely, anti-inflammatory mediator IL-10 mRNA was down-regulated in both organs. These results suggest that imidacloprid cause oxidative stress and inflammation in central nervous system and liver in non-target organisms in rats.
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