Kidney Lipid Peroxidation Levels Research Articles

Effects of date seeds administration on anxiety and depressive symptoms in streptozotocin-induced diabetic rats: biochemical and behavioral evidences.

Several epidemiological data indicate that chronic hyperglycemia is associated with behavioral changes such as anxiety and depressive symptoms. Date seeds, one of the most potent products with potential antioxidant activities and possess many benefits against hyperglycemia and its complication. The aim of the current study was to explore the potential effect of date seeds extract on biochemical and behavioral changes (anxiety and depression) in streptozotocin (STZ)-diabetic rats. Rats were divided into four groups as follows: normal control, diabetic control, diabetic treated with the lyophilized aqueous extract of the date seed (2,000mg/kg) (LAE-DS) and diabetics treated with insulin (4UI/day). Experimental diabetes was induced by a single intraperitoneal injection of STZ (60mg/kg). After 24days treatment period, anxiety and depressive behaviors were evaluated using four behavioral tests. After sacrifice, blood samples were collected to evaluate lipid parameters. In addition, rat organs (kidney, liver and brain) were dissected out in order to estimate lipid peroxidation levels as oxidative stress marker. Oral administration of the lyophilized aqueous extract of date seeds and insulin injection for 30days significantly decreased blood glucose levels in STZ-diabetic rats and protected them against undesirable changes in lipid parameters, including cholesterol, triglycerides, LDL cholesterol, VLDL cholesterol and atherosclerosis index. Compared to untreated diabetic rat, a significant decrease in lipid peroxidation levels in kidney, liver and brain (Hippocampus and prefrontal cortex) were observed after treatment with insulin or LAE-DS in diabetic rats. Furthermore, insulin and LAE-DS administration prevented anxiety-related behaviors in STZ-diabetic rats. Therefore, it would be possible to combine this extract with insulin and use it as an antioxidant supplement for type 1 diabetic patients.

Can Juniperus communis L. oil improve nephropathy in diabetic rats

Objective: Juniperus communis L. is a shrub belonging to family Cupressaceae L. mainly growth in Eurasia. The antioxidant and antidiabetic activity of aqueous extract of J. communis L. berries indicated benefits as a potent antidiabetic in streptozotocin induced diabetic albino rats. This study was carried out to determine whether J. communis L. oil supplement will effectively manage renal dysfunction in diabetic rats.Methods: Twenty eight rats were divided into 4 equal groups as follows; control group, diabetic group, J. communis L. oil (200 mg/kg) treated group, and diabetic+J. communis L. oil (200 mg/kg) treated group. At the end of the experimental period, all rats were sacrificed and renal function parameters such as kidney antioxidant and lipid peroxidation markers and serum creatinine, serum urea, blood urea nitrogen (BUN), and serum total protein levels were measured in all groups. Results: HbA1c, serum glucose, serum urea, serum creatinine, BUN, and kidney lipid peroxidation levels increased but serum total protein and antioxidant levels decreased in diabetic group comparing with control group (p<0.05). Furthermore, HbA1c, serum glucose, serum urea, serum creatinine, BUN, and kidney lipid peroxidation levels decreased and also, serum total protein and antioxidant levels increased in diabetic group treated with J. communis L. oil comparing with diabetic group (p<0.05). Conclusion: This study has provided direct evidence of a link between diabetes mellitus and diabetic nephropathy and demonstrated that J. communis L. oil provide a protective effect on the kidney as evidenced by an improvement of the renal function tests as well as reduction in oxidative stress parameters.

Agomelatine reduces brain, kidney and liver oxidative stress but increases plasma cytokine production in the rats with chronic mild stress-induced depression

Agomelatine (AGOM) as an antidepressant acts both as a melatonin-receptor agonist and a selective serotonin-receptor antagonist. As a potent melatonin derived antioxidant, AGOM might modulate depression-induced lipid peroxidation and pro-inflammatory cytokines in brain, kidney and liver. The present study explores whether AGOM protects against experimental depression-induced brain, kidney and liver oxidative stress, and plasma cytokine production in rats with chronic mild stress (CMS)-induced depression. Thirty-six rats were divided into four groups. The first group was used as an untreated control. The second group received AGOM for 4weeks. The third group was exposed to chronic mild stress (CMS) of 4weeks for induction depression. The fourth group received 40mg/kg AGOM and CMS for 4weeks. Liver and kidney lipid peroxidation levels were high in the CMS group although they were low in AGOM treatments. AGOM and AGOM+CMS treatments increased the lowered glutathione peroxidase activity and reduced glutathione levels in brain, kidney and liver of CMS group. β-carotene, vitamin A and vitamin E concentrations in the brain, kidney and liver of the four groups were not changed by CMS and AGOM treatments. However, plasma TNF-α, interleukin (IL)-1β, and IL-4 levels were high in the CMS and AGOM group and their levels were further increased by the AGOM+CMS treatment. In conclusions, AGOM induced protective effects against experimental depression-induced brain, kidney, and liver oxidative injuries through regulation of the glutathione concentrations and glutathione peroxidase activity. However, plasma cytokine productions were increased by the AGOM treatment.

Zinc Supplementation Attenuates Metallothionein and Oxidative Stress Changes in Kidney of Streptozotocin-Induced Diabetic Rats

Zinc is an element that under physiological conditions preferentially binds to and is a potent inducer of metallothionein under physiological conditions. The present study was conducted to explore whether zinc supplementation morphologically and biochemically protects against diabetic nephropathy through modulation of kidney metallothionein induction and oxidative stress in streptozotocin-induced diabetic rats. Thirty-two Wistar albino male rats were equally divided into four groups. The first group was used as untreated controls and the second group was supplemented with 30mg/kg/day zinc as zinc sulfate. The third group was treated with streptozotocin to induce diabetes and the fourth group was treated with streptozotocin and supplemented with zinc as described for group 2. The blood glucose and micro-albuminuria levels, body and kidney weights were measured during the 42-day experimental period. At the end of the experiment, the kidneys were removed from all animals from the four groups. Diabetes resulted in degenerative kidney morphological changes. The metallothionein immunoreactivity level was lower and the kidney lipid peroxidation levels were higher in the diabetes group than in the controls. The metallothionein immunoreactivity levels were higher in the tubules of the zinc-supplemented diabetic rats as compared to the non-supplemented diabetic group. The zinc and metallothionein concentrations in kidney tissue were higher in the supplemented diabetic group compared to the non-supplemented diabetes group. The activity of glutathione peroxidase did not change in any of the four groups. In conclusion, the present study shows that zinc has a protective effect against diabetic damage of kidney tissue through stimulation of metallothionein synthesis and regulation of the oxidative stress.

Protection against cisplatin-induced nephrotoxicity in mice by Curcuma comosa Roxb. ethanol extract

The protective effect of an ethanol extract of Curcuma comosa against cisplatin-induced renal toxicity in mice was studied. Adult male mice were pretreated for 4 days with the ethanol extract of C. comosa [100-200 mg/kg body weight (BW), orally (p.o.)] before injection of cisplatin (12.5 mg/kg BW, intraperitoneally (i.p.)). Five days later the mice were killed, and blood samples were collected to determine blood urea nitrogen (BUN) and plasma creatinine levels. Kidneys were examined histopathologically and levels of lipid peroxidation, gluthathione (GSH) content, and superoxide dismutase (SOD), gluthathione peroxidase (GPx), and catalase (CAT) activities were determined. Histological examinations revealed degenerative changes and tubular necrosis in mice treated with cisplatin, which were improved by pretreatment with C. comosa ethanol extract. Cisplatin raised BUN, creatinine, and kidney lipid peroxidation levels, and lowered kidney GSH content and levels of GPx, SOD, and CAT activities, all of which (except SOD and CAT) could be restored to normal values by pretreatment with 200 mg/kg BW of C. comosa ethanol extract. In addition, the ethanol extract of C. comosa and its isolated diarylheptanoid compound also exhibited radical scavenging activities. The results suggest that the ethanol extract of C. comosa exhibits effective protection against cisplatin-induced nephrotoxicity mediated through its antioxidant activity.

Green Tea Drinking Reduces the Effects of Vanadium Poisoning in Rat Kidney

Transitional metals, as vanadium, are known to exert noxious effects by generating oxidative stress. Addition of antioxidants in the diet could decrease the cytotoxic effect related to the oxidative stress. The present study, carried out in rats, is a contribution to explore mechanisms underlying vanadium toxicity and possible protective effects of green tea Camellia sinensis which is known to be rich in antioxidant compounds (polyphenols...). Chronic intoxication by vanadium given in drinking water was found to induce histological structure changes of renal glomeruli and tubules, but indicators of nephrotoxicity (serum creatinine and urea, urinary pH) were not perturbed. Vanadium accumulation was found to be decreased in (T+V) group, and renal histological changes were not observed. The ability of catechins to chelate metal ions, and perhaps vanadium, could explain protective effects of herbal green tea. Intraperitoneal administration of vanadium to rats (V) was found to induce an increase of lipid peroxidation levels in kidney, that was lowered in rats (T+V) drinking herbal tea. This effect was partly due to a tea-induced decrease of basal lipid peroxidation level in kidney tissues. Similar HSP72 underexpression and HSP73 overexpression were found in (V) and (T+V) rats. Vanadium-induced HSP70 underexpression was discussed in relation to the ability of the metal to inactivate some phosphatases, resulting in phosphorylation and transcriptional activity changes of heat shock factor 1 (HSF1). Besides, two forms of GRP94 (96, 98kD) were immunodetected, that appeared inversely regulated by vanadium, but not by herbal tea. This suggests that vanadium can disrupt reticulum endoplasmic function resulting in GRP94 phosphorylation and/or glycosylation changes.

Changes in Antioxidant Status and Biochemical Indices after Acute Administration of Artemether, Artemether‐Lumefantrine and Halofantrine in Rats

Artemether, artemether-lumefantrine, or coartem and halofantrine are alternative antimalarial drugs to chloroquine. Their efficacy and potential to delay drug resistance in falciparum malaria had led to their increased use. Although these drugs have proven to be well tolerated, there are adverse effects associated with them. This study was designed to examine the toxic potential of acute administration of these drugs in rats. Twenty-four rats were divided into four groups: group I (control) received distilled water; group II received artemether for 5 days with an initial dose of 3.2 g/kg body weight on day 1 and 1.6 mg/kg body weight on days 2-5; group III received coartem (27 mg/kg body weight/day) for 3 days, which was divided into two equal portions per day; and group IV received halofantrine (24 mg/kg body weight/day) in three equal portions. Administration of artemether, coartem and halofantrine caused significant decrease (P < 0.05) in reduced glutathione levels in the liver by 29%, 21% and 26%, respectively. In contrast, there were no significant differences (P > 0.05) in the kidney glutathione levels. Furthermore, artemether, coartem and halofantrine decreased the liver- and kidney-enzymatic antioxidant status of the animals. Precisely, artemether, coartem and halofantrine decreased liver superoxide dismutase and catalase activities by 45%, 50% and 57%; and 20%, 29% and 23%, respectively. While the kidney catalase activities were decreased by 41%, 28% and 30%, respectively, the drugs however did not produce significant effect (P > 0.05) on the kidney superoxide dismutase activities. In addition, artemether, coartem and halofantrine decreased the hepatic levels of glutathione S-transferase by 64%, 51% and 53%, respectively. Administration of artemether, coartem and halofantrine significantly increased (P < 0.05) liver and kidney lipid peroxidation levels by 67%, 50% and 81%; and 58%, 43% and 31%, respectively. This indicates that the liver is considerably more affected than the kidneys. Similarly, halofantrine treatment caused significant elevation (P < 0.05) in the levels of serum creatinine, aspartate and alanine aminotransferases and blood urea nitrogen by 73%, 66%, 61% and 63%, respectively. These data indicate that oral administration of artemether, coartem and halofantrine has adverse effects on both enzymic and non-enzymatic antioxidant status of the animals.

Effects of Z-FA.FMK on d-galactosamine/tumor necrosis factor-alpha-induced kidney injury and oxidative stress in mice

The aim of this investigation was to demonstrate that benzyloxicarbonyl-L-phenylalanyl-alanine-fluoromethylketone (Z-FA.FMK), which is a pharmacological inhibitor of cathepsin B, has protective role on the kidney injury that occurs together with liver injury. Methods BALB/c male mice used in this study were divided into four groups. The first group was given physiologic saline only, the second group was administered Z-FA.FMK alone, the third group received D: -galactosamine and tumor necrosis factor-alpha (D-GalN/TNF-alpha), and the fourth group was given both D-GalN/TNF-alpha and Z-FA.FMK. One hour after administration of 8 mg/kg Z-FA.FMK by intravenous injection, D-GalN (700 mg/kg) and TNF-alpha (15 microg/kg) were given by intraperitoneal injection. Results In the group given D-GalN/TNF-alpha, the following results were found: severe degenerative morphological changes in the kidney tissue, a significant increase in the number of activated caspase-3-positive tubular epithelial cell, an insignificant increase in the number of proliferating cell nuclear antigen (PCNA)-positive tubular epithelial cell, a decrease in the kidney glutathione (GSH) levels, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, an increase in the kidney lipid peroxidation (LPO) levels, lactate dehydrogenase (LDH) activity, serum aspartate aminotransferase (AST), and alanine aminotransferase (ALT) activities, uric acid and urea levels. In contrast, in the group given D-GalN/TNF-alpha and Z-FA.FMK, a significant decrease in the D-GalN/TNF-alpha-induced degenerative changes, a decrease in the number of activated caspase-3-positive tubular epithelial cell, a insignificant decrease in the number of PCNA-positive tubular epithelial cell, an increase in the kidney GSH levels, CAT, SOD and GPx activities, a decrease in the kidney LPO levels, LDH activity, serum AST and ALT activities, uric acid and urea levels were determined. Conclusion These results suggest that pretreatment with Z-FA.FMK markedly lessens the degree of impairment seen in D-GalN/TNF-alpha-induced kidney injury, which occurred together with liver injury in mice.

LIPID PEROXIDATION AND ANTIOXIDANT ENZYME ACTIVITY IN DIFFERENT ORGANS OF MICE EXPOSED TO LOW LEVEL OF MERCURY

The effects of mercuric chloride (Hg) on lipid peroxidation (LPO), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD) and glutathione (GSH) levels in different organs of mice (CD-1) were evaluated. Mice were exposed (2 days/week) to 0.0 (control), 0.8 (low) and 8.0 (mid) and 80.0 (high) gHg/kg/day for 2 weeks. The high dose group was excluded from the study due to high mortality. LPO levels in kidney, testis and epididymus at low and mid doses; GR and GPx levels in testis at mid dose; SOD levels in brain and testis at both doses, liver and epididymus at mid dose; GSH levels in testis at both doses were significantly increased compared to their controls. However, the GR levels in kidney at both doses and in epididymus at mid dose; GPx levels in kidney and epididymus and SOD levels in kidney at both the doses; GSH levels in epididymus at mid dose were significantly decreased compared to their control. Body weight gain and food efficiency were significantly reduced (<0.05) in mid dose. These results indicated that Hg treatment enhanced LPO in all tissues, but showed significant enhancement only in kidney, testis and epididymus suggesting that these organs were more susceptible to Hg toxicity. The increase in antioxidant enzyme levels in testis could be a mechanism protecting the cells against reactive oxygen species.

Effect of coenzyme Q10 on the survival time and lipid peroxidation of adriamycin (doxorubicin) treated mice.

The effect of coenzyme Q10 (Co Q10) was examined on the survival time and lipid peroxidation of adriamycin (ADM)-treated ICR mice. Co Q10 showed a protective effect against a subacute toxicity in mice induced by two intraperitoneal administrations of ADM (15 mg/kg). The group treated orally with 10 mg/kg of Co Q10 showed the longest survival time of all the groups studied (16.81 +/- 10.29 days, mean +/- S.D.) and a significantly longer survival time (p less than 0.001) than the ADM-alone group (7.48 +/- 1.99 days). The inhibitory effect of Co Q10 on the plasma and tissue lipid peroxidation levels did not correlate with the effect of prolonging the survival time of mice. Co Q10 tended to inhibit rises in plasma and liver lipid peroxidation levels induced by ADM administration, but there was no statistically significant difference between treatments. There was a statistically significant different inhibitory effect in the kidney lipid peroxidation levels, but was not in those of the heart.