Protective Effect of Quercetin and Ginger (Zingiber officinale) Extract against Dimethoate Potentiated Fluoride-Induced Nephrotoxicity in Rats.

This study aimed to determine the potential of quercetin and Zingiber officinale (ZO) Roscoe extract to alleviate the renal damage induced by dimethoate (DM) and fluoride (F-) alone and by their combined exposure in rats. A total of 54 adult Wistar rats were randomly allocated to nine groups (n = 6). A sub-lethal dose of DM (1/10th of the median lethal dose) was administered by oral gavage alone and along with F- (4.5 ppm, three-fold the permissible limit) in their drinking water continuously for 28 days. Chromatographical analysis revealed the presence of quercetin, curcumin, and other phytochemicals with strong antioxidant properties in ZO-rhizome extract. Severe changes were observed in the levels of the renal biomarkers and histoarchitecture after co-administration of the toxicants, indicating greater kidney damage. The administration of ZO extract (300 mg/kg) along with either or both toxicants led to a significant restoration of the biochemical markers and renal antioxidant profile and histology.

Dose-Dependent Oxidative Damage in Erythrocytes and Hepatic Tissue of Wistar Rats Concurrently Exposed with Arsenic and Quinalphos: a Subacute Study.

Concurrent exposure to a multitude of environmental toxicants pose serious health hazard to humans and animals. The present investigation was conceptualized to determine deleterious effects of concomitant subacute arsenic and quinalphos exposure on antioxidant responses of liver and erythrocytes of Wistar rats. Fifty-four Wistar rats were divided into nine groups with six animals in each. Animals were exposed to either quinalphos (1/100th and 1/10th of LD50) through oral gavage daily or arsenic (50 and 100 ppb) in drinking water alone and in combination for 28 days. While treatment with different toxicants alone also significantly reduced hemoglobin concentration, hepatic biomarkers and levels of antioxidant parameters as compared with control values, concomitant exposure significantly (P < 0.05) elevated levels of hepatic transaminases and alkaline phosphatase. Moreover, along with significant depletion in activities of SOD, CAT, TTH, AChE, and enzymes of glutathione complex, a significant enhancement of lipid peroxidation was also recorded in liver and erythrocytes in co-exposed animals in a dose-dependent manner when compared with exposure to individual toxicant. More severe alterations occurred in hepatic histo-architecture of rats receiving combined treatment as compared with those treated with either toxicant. Results indicated that oxidative damage in erythrocytes was more than that of the liver of rats on concomitant exposure of arsenic and quinalphos in a dose-dependent manner. In nutshell, our results revealed that combined treatment of quinalphos with arsenic potentiated toxic effects of either toxicant on antioxidant machinery of liver and erythrocytes and hepatic histomorphology of exposed Wistar rats.

Evaluation of the wound healing activity of ethanolic extract of Bergenia ciliata (Haw.) Sternb. rhizome with excision wound model in Wistar rats.

ETHNOPHARMACOLOGICAL RELEVANCE: Bergenia ciliata (Haw.) Sternb. is a plant growing in the Himalayan region of India where locals use its rhizomes for a variety of disease conditions including wounds and fractures. Although some of its pharmacological benefits have been documented, scientific validation of its wound healing property has not been done so far. AIM OF THE STUDY: To ensure use of this natural remedy as an alternative therapy to the faster wound healing, this study evaluated the wound healing activity of the ethanolic extract of Bergenia ciliata rhizome using excision wound model in Wistar rats. MATERIAL AND METHODS: Four groups (n = 10) of rats were subjected to different topical wound regimens for 14 days. Simple paraffin-lanolin ointment was applied to the control group rats. One group was applied povidone-iodine 10% (w/w) ointment. The other two groups were treated with ointment of ethanolic extract of Bergenia ciliata at 5 or 10% (w/w) rhizome, respectively. Blood and wound tissue samples were collected on 7th and 14th day of treatment and were correspondingly subjected to histopathology, and the assays of L-hydroxyproline, D-glucosamine, antioxidants and pro-inflammatory cytokines. RESULTS: Wound histology revealed increased collagenation, re-epithelialization and neovascularization while decreased bacterial colonies in the treatment groups. These histological changes and wound contraction were better in the 10% Bergenia ciliata group. Tissue L-hydroxyproline levels, blood enzymatic and non-enzymatic antioxidants were increased in the treatment groups. On 7th day of treatment glucosamine levels increased in the treatment groups, while as a reverse trend was observed on day 14. Plasma levels of TNF-α and IL-6 decreased in the treatment groups. CONCLUSIONS: The results indicate that treatment with Bergenia ciliata extract ointment provides satisfactory wound healing which is comparable to that of the standard wound healing ointment, povidone-iodine and is surpassing simple lanolin-paraffin ointment. The improved wound healing, especially in the 10% Bergenia ciliata groups, can be attributed to satisfactory profile of the above studied parameters in these treatment groups which is also construed by the phytochemical analysis of its extract revealing the presence of antioxidant and anti-inflammatory compounds gallic acid, catechin, quercetin and rutin as the major active components.

Neuroprotective potential of hydroethanolic hull extract of Juglans regia L. on isoprenaline induced oxidative damage in brain of Wistar rats.

The study was aimed at assessing isoprenaline (ISO) induced oxidative damage in brain of Wistar rats and its protection by hydroethanolic hull extract of Juglans regia. Administration of ISO significantly increases catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR), malondialdehyde (MDA) and advanced oxidation protein product (AOPP) levels and significantly reduced activities of antioxidant status (TAS), total thiols (TTH), acetylcholinesterase (AChE), arylesterase (AE), and glutathione peroxidase (GPx) in rat brain. Histopathologically, neuronal degeneration, spongiosis and gliosis were seen in cerebral cortex after ISO administration. Pretreatment with hull extract restored TAS, TTH, AChE, CAT and SOD values. Additionally, significant reductions were noted in levels of MDA, AOPP, and severity of histomorphological changes in cerebral cortex following hull extract treatment. Altered antioxidant biomarkers along with histopathological changes indicate oxidative injury in rat brain following ISO administration. Repeated administration of J. regia hull extract demonstrating presence of neuroprotective properties against ISO induced oxidative damage in rat brain.

Maximum contaminant level of arsenic in drinking water potentiates quinalphos-induced renal damage on co-administration of both arsenic and quinalphos in Wistar rats.

This study was designed to determine alterations in renal biomarkers, antioxidant profile, and histomorphology of renal tissue following subacute exposure to quinalphos alone or in conjunction with arsenic in rats. A total of 54 adult Wistar rats were randomly divided into nine groups of six rats each and were administered sub-lethal concentrations of quinalphos (1/100th and 1/10th of LD50) orally daily and arsenic (50 and 100 ppb) in drinking water for 28 days. Significantly (p < 0.05) decreased levels of antioxidant biomarkers in renal tissue, viz., total thiols, catalase, superoxide dismutase, glutathione peroxidase, glutathione-s-transferase, and glutathione reductase along with increased (p < 0.05) thiobarbituric acid reacting substance (TBRAS) levels indicated that significant oxidative damage to renal tissue occurred following repeated administrations of quinalphos at either dose levels or arsenic at the concentration of 100 ppb when compared with the control rats. The alterations in the antioxidant parameters were observed to be more pronounced in co-administered groups as compared with either toxicant administered group. Similarly, activity of renal acetylcholinesterase was decreased after repeated exposure to quinalphos or arsenic, but inhibition was higher (up to 48%) in rat renal tissue co-exposed with quinalphos and arsenic at the higher concentration. These findings corroborated with the histopathological alterations in renal tissue of toxicant exposed rats. The altered plasma and tissue antioxidant biomarkers along with histopathological changes in the kidney at higher dose level of either toxicant indicate that renal tissue is significantly impacted by these toxicants, and these effects become more pronounced after their co-administration.

Potential of Juniperus communis L as a nutraceutical in human and veterinary medicine.

Plants have been used for thousands of years as medicine for treating variety of diseases and medical complaints by most of the civilizations. Juniperus communis L. is an evergreen aromatic shrub with high therapeutic potential for the treatment of diseases in human and animals. The plant is rich in aromatic oils, invert sugars, resins, catechin, organic acid, terpenic acids, leucoanthocyanidin, alkaloids, flavonoids, tannins, gums, lignins, wax, etc. Juniper berries or extract of the plant has traditionally been used as diuretic, anti-arthritis, anti-diabetes, antiseptic as well as for the treatment of gastrointestinal and autoimmune disorders. The essential oil and extracts of juniper have been experimentally documented to have antioxidant, antibacterial, antiviral and antifungal activities. Recent studies have also found anti-inflammatory, cytotoxic, hypoglycemic and hypolipidemic effects of berries in experimental models. Further, the essential oil incorporation retarded lipid peroxidation in preserved meat due to its high antioxidant effect which not only improved meat product quality but also improved shelf life of the product. Thus natural antioxidant such as juniper can be used in place synthetic antioxidant for the preservation and improving self-life of meat products. New well designed clinical trials in human and animals using well-characterized J. communis extract or oil need to be conducted so that additional information is generated which can support the use of this natural product as a nutraceutical.

Effect of bifenthrin on oxidative stress parameters in the liver, kidneys, and lungs of rats.

Oxidative stress inducing potential of bifenthrin was evaluated in the liver, kidney, and lung of rats following its repeated oral administration for 20 and 30 days. Bifenthrin-treated rats showed a significant lipid peroxidation in all three tissues. By 20th day of treatment, there was a significant decrease in superoxide dismutase activity of the liver, catalase and glutathione peroxidase activity of the liver and lung, and glutathione S-transferase activity of the kidney and lung. By 30th day of exposure, the activities of these enzymes were significantly decreased in all three tissues. The highest oxidative stress, indicated by lipid peroxidation and alteration in antioxidant enzymes, is produced in the liver followed by the kidney and lung. In conclusion, bifenthrin has a potential to induce severe oxidative stress in the liver, kidney, and lung. The extent of oxidative stress is increased with the duration of exposure.

Alteration in thiols homeostasis, protein and lipid peroxidation in renal tissue following subacute oral exposure of imidacloprid and arsenic in Wistar rats.

The aim of present study was to assess whether No Observed Effect Level (NOEL) of imidacloprid (IMI) potentiates the arsenic induced renal toxicity at its maximum contaminant level in drinking water in Wistar rats. Significant elevation of lipid and protein oxidation with reduced level of total thiols and antioxidant enzymes (catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase and glutathione-s-transferase) in renal tissue may have contributed to increased renal plasma biomarkers (creatinine and blood urea nitrogen) following repeated exposure of IMI and arsenic alone and in-combination. The altered renal biomarkers in co-exposed groups corroborated with histopathological alterations in renal tissue. The observations indicated that altered thiol homeostasis in renal tissue may be associated with increased lipid and protein oxidation in IMI and arsenic administered rats. It is concluded that administration of IMI potentiate the arsenic induced renal damage in Wistar rats.

Potentiating effect of imidacloprid on arsenic-induced testicular toxicity in Wistar rats.

BACKGROUND: It is an established fact that humans and animals are exposed to more than one chemical concurrently from various sources such as food, air and water. In the past, much emphasis was laid on evaluating the toxic effects of a single chemical. Nowadays an increased attention is being paid to the interaction of xenobiotics with one another. Therefore, a study was aimed to evaluate the potentiating effect of imidacloprid (IMI) on arsenic-induced testicular toxicity in rats. METHODS: Adult male Wistar rats randomly divided into eight groups with six in each were subjected to daily oral administrations for 28 days. Group I served as control, group II received IMI at the dose rate of 16.9 mg/kg body weight, group III, IV and V received arsenic at the dose rate of 50, 100 and 150 ppb in drinking water whereas group VI, VII and VIII received both arsenic and IMI. RESULTS: Repeated oral administrations of IMI or arsenic (150 ppb) alone resulted in a significant (P < 0.05) elevation in the levels of malondialdehyde (MDA) and advanced oxidation protein product (AOPP) along with significant (P < 0.05) decline in total thiols and antioxidant enzymatic activities indicating reduced antioxidant defense in testicular tissue of exposed rats. These findings were further corroborated with histological alterations in testes like fluid accumulation in interstitial spaces in IMI administered rats. Similarly, rats provided access exclusively to arsenic-containing drinking water induced degenerative changes in seminiferous tubules in a concentration-dependent manner. Concurrent administration of IMI and arsenic produced more severe antioxidant and histopathological alterations of testes as compared to exposure to either toxicant. CONCLUSIONS: Reduced antioxidant activities, increased MDA and AOPP levels with severe histopathological alterations in testes of rats on concurrent exposure indicated that IMI potentiated the arsenic-induced testicular toxicity in Wistar rats.

Toxic effects of imidacloprid combined with arsenic: Oxidative stress in rat liver.

Imidacloprid (IMI), a newer neonicotinoid insecticide, induces oxidative insult to hepatocytes due to the formation of reactive metabolites during hepatic metabolism. The present study aimed to determine the potentiating effect of arsenic (As) on IMI-induced hepatic damage in Wistar rats. Rats, randomly divided into eight groups with six in each, were subjected to daily oral administration for 28 days. Group I served as control; group II received IMI at the dose rate of 16.9 mg/kg body weight; groups III, IV, and V received As at the dose rate of 50, 100, and 150 ppb, respectively, in drinking water; groups VI, VII, and VIII received both IMI (16.9 mg/kg) and As in drinking water at the rate of 50, 100, and 150 ppb, respectively. Repeated oral administration of IMI or As resulted in significant ( p < 0.05) elevation of plasma phosphatases, transferases, hepatic malondialdehyde, and advanced oxidation protein product levels, but significantly ( p < 0.05) decreased levels of total proteins, thiols, and activities of antioxidant enzymes that indicate oxidation-induced hepatotoxicity. These findings were further corroborated by histological alterations in hepatic tissue of IMI or As-administered rats. The coadministration of both IMI and As in rats produced more severe alterations in these parameters in hepatic tissue. Reduced antioxidant indices and increased hepatic damage biomarkers with pronounced histopathological alterations in hepatic tissue after combined exposure to toxicants indicate potentiating toxic effect of As on IMI-induced hepatotoxicity.

Effect of deltamethrin and fluoride co-exposure on the brain antioxidant status and cholinesterase activity in Wistar rats.

The study evaluated the effect of commercial preparation of deltamethrin, Butox®, and fluoride (F-) co-exposure on the brain antioxidant status and cholinesterase activity in rats. Group A was untreated. Group B was gavaged Butox®, providing deltamethrin at the dose rate of 1.28 mg per kg body weight per day. Group C was administered F-, as NaF, in drinking water providing 20 ppm F-. Group D received both deltamethrin and F- at the same dosages as groups B and C, respectively. Although, glutathione S-transferase activity was induced only in Butox® alone treated group, the activities of superoxide dismutase and catalase were inhibited in all treatment groups when compared to the control group. Elevated lipid peroxidation was observed in the groups exposed to F-. The activity of erythrocyte acetylcholinesterase (AChE) was inhibited in Butox® treated groups, whereas brain AChE activity was inhibited in all treatment groups. In conclusion, both deltamethrin (given as Butox®) and F- inhibit AChE activity and produce oxidative stress in brain with F- producing more oxidative damage. However, compared to the individual exposures, the co-exposure of these chemicals does not produce any exacerbated alteration in these biochemical parameters.

Hypoglycemic, Hypolipidemic, and Wound Healing Potential of Quercetin in Streptozotocin-Induced Diabetic Rats.

BACKGROUND: Among the dietary polyphenolic, quercetin is the most common compound available in vegetables and fruits. The phytochemicals are used to treat diabetic wounds and diabetes, and specifically dietary polyphenols are being extensively studied for their anti-inflammatory and antioxidant abilities. OBJECTIVE: The objective of the study was to assess the hypoglycemic, hypolipidemic, and wound healing potential of quercetin in streptozotocin (STZ)-induced diabetic Wistar rats. MATERIALS AND METHODS: Induction of diabetes was done by intraperitoneally administration of STZ at the dose of 55 mg/kg in Wistar rats. An excision wound was created in diabetic rats that were treated with quercetin (100 mg/kg) orally and quercetin ointment topically to evaluate the antidiabetic and wound healing potential of quercetin. RESULTS: Repeated oral administration of quercetin along with topical application of quercetin ointment in diabetic rats normalized the altered blood glucose, hydroxyproline, and glucosamine levels. Topical application of quercetin ointment alone on the excised wound was sufficient enough to heal the wound area in diabetic rats. CONCLUSIONS: The result of the present study indicates that quercetin produces hypoglycemic effect in STZ-induced diabetic rats and normalized plasma lipids and protein profiles. Besides, this quercetin also has an excellent wound healing property when applied topically on the wound area in diabetic rats. SUMMARY: Quercetin has hypoglycaemic and hypolipidemic potential in streptozotocin induced diabetes in wistar ratsDermal application along with oral administrations of quercetin has more effective in wound healing in diabetic animalsHistopathological studies of pancreas, skin and liver shows significant reduction in archaeological alterations on quercetin administrations in diabetic rats. Abbreviation used: STZ: Streptozotocin; CMC: Carboxy methyl cellulose; HDL: High density lipoproteins; LDL: low density lipoproteins.

Free radical-induced nephrotoxicity following repeated oral exposureto chlorpyrifos alone and in conjunction with fluoride in rats.

BACKGROUND/AIM: Chronic renal disorder is becoming a major health problem worldwide. The purpose of the present study was to investigate alterations in the renal antioxidant system in rats induced by repeated exposure to chlorpyrifos (CPF) alone and in conjunction with fluoride. MATERIALS AND METHODS: Wistar rats were randomly allocated to seven groups, each consisting of six rats, and were subjected to different treatment regiments for 28 days. RESULTS: Significant increases (P < 0.05) in plasma protein, blood urea nitrogen, and creatinine levels indicated alterations in renal functions on repeated exposure to CPF or fluoride; moreover, these changes were more pronounced in animals exposed to both toxicants concurrently. A significant increase (P < 0.05) in malondialdehyde levels and decreases in superoxide dismutase, catalase, and glutathione peroxidase activities in renal tissue were noted, indicating renal damage on exposure to CPF, fluoride, or the combination of those. CONCLUSION: Our observations suggested that the concurrent exposure to CPF and fluoride increased the extent of renal damage. These findings indicate that this damage is due to increased free radical formation and a reduced function of the antioxidant system in renal tissue. Thus, the application of CPF as an insecticide should be reduced in areas where the fluoride levels in ground waters are high in order to minimize renal damage in exposed populations.

Total antioxidant and oxidant status of plasma and renal tissue of cisplatin-induced nephrotoxic rats: protection by floral extracts of Calendula officinalis Linn.

The present study was aimed to determine the total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI) of plasma and renal tissue in cisplatin (cDDP) induced nephrotoxic rats and its protection by treatments with floral extracts of Calendula officinalis Linn. Treatment with cDDP elevated (p < 0.05) the levels of blood urea nitrogen, creatinine (CR), TOS, OSI and malondialdehyde (MDA) but lowered (p < 0.05) total plasma proteins, TAS, total thiols (TTH), blood glutathione (GSH) and antioxidant enzymes compared to the control group. Pre- and post-treatments of ethanolic floral extract of C. officinalis along with cDDP restored (p > 0.05) CR, albumin, TOS, GSH and activities of antioxidant enzymes in blood and renal tissue. Ethanolic extract treatments reduced (p < 0.05) MDA level in renal tissue without restoring the erythrocyte MDA level following cDDP treatment. These observations were further supported by the histopathological findings in renal tissue. Observations of the present study have shown that treatments with ethanolic floral extract of C. officinalis protect cDDP induced nephrotoxicity by restoring antioxidant system of the renal tissue.

Hepatotoxicity Induced by Subchronic Exposure of Fluoride and Chlorpyrifos in Wistar Rats: Mitigating Effect of Ascorbic Acid.

The aim of the study was to investigate the ameliorative properties of ascorbic acid against the subchronic effect of co-exposure of fluoride (F) and chlorpyrifos (CPF) on oxidative damage markers such as lipid peroxidation (MDA) and antioxidant defense system in the liver of adult Wistar rats. The animal groups were provided with either vehicle or ascorbic acid (60 mg/kg, b.w.) or NOAEL dose of fluoride (1 ppm) or CPF (1 mg/kg, b.w.) or ten times of such doses orally alone and in combination or pre-treated with ascorbic acid along with co-exposure of F and CPF every consecutive day for 28 days. Hepatic damage marker analysis in blood revealed that aspartate and alanine aminotransferases, alkaline phosphatase, and lactate dehydrogenase were significantly (P < 0.05) increased with single or combined exposure of F or CPF at either dose levels. Significant increased oxidative damage of hepatocytes as indicated by increased MDA levels with decrease in tissue ascorbate and free radical scavenging enzymes like catalase, superoxide dismutase, and glutathione peroxidase was observed in groups treated with either F or CPF as well as in combinedly treated animals as compared to control animals. Supplementation of ascorbic acid restored the hepatic specific marker enzymes in blood following co-exposure of F and CPF at lower doses which were otherwise increased in the F and CPF co-exposed rats. The results show that ascorbic acid supplementation with F and CPF prevents or diminishes the hepatic damage in rats co-exposed to toxicants and may act as a putative protective agent against toxicant-induced liver tissue injury.

Sub-acute deltamethrin and fluoride toxicity induced hepatic oxidative stress and biochemical alterations in rats.

The current study investigated the effects of deltamethrin, fluoride (F(-)) and their combination on the hepatic oxidative stress and consequent alterations in blood biochemical markers of hepatic damage in rats. Significant hepatic oxidative stress and hepatic damage were observed in the toxicant exposed groups. These changes were higher in the deltamethrin-F(-) co-exposure treatment group, depicting a positive interaction between the two chemicals.

Effect of repeated oral administration of bifenthrin on lipid peroxidation and anti-oxidant parameters in Wistar rats.

The oxidative stress-inducing potential of the pyrethroid insecticide, bifenthrin, was evaluated in rats at 5.8 mg/kg body weight once daily for 20 or 30 days. Bifenthrin treated animals showed significantly increased lipid peroxidation, evidenced by increased blood malondialdehyde levels. Blood glutathione levels and activities of catalase and glutathione peroxidase decreased significantly in the bifenthrin treated animals after both 20 and 30 days of treatment, whereas, the activities of superoxide dismutase and glutathione S-transferase decreased significantly only on the 30th day. In conclusion, bifenthrin has a potential to induce severe oxidative stress in rats exposed to sublethal concentrations.

Plasma pharmacokinetics and milk levels of ceftriaxone following single intravenous administration in healthy and endometritic cows.

Pharmacokinetics and milk levels of ceftriaxone were studied in healthy and endometritic cows following single intravenous administration. The drug was detected up to 8 h of dosing in plasma of healthy and endometritic cows and the drug disposition followed three-compartment open model. The values of Vd(area), AUC, t(1/2beta), Cl(B), MRT and P/C ratio were 0.50 +/- 0.19 L.kg(-1), 62.2 +/- 23.3 microg.ml(-1).h, 1.02 +/- 0.07 h, 0.30 +/- 0.09 L.kg(-1).h(-1), 1.55 +/- 0.25 h and 0.52 +/- 0.27, respectively, in healthy and 1.55 +/- 0.52 L.kg(-1), 37.0 +/- 17.1 microg.ml(-1).h, 1.56 +/- 0.25 h, 0.56 +/- 0.14 L.kg(-1).h(-1), 2.14 +/- 0.34 h and 1.44 +/- 0.60, respectively, in endometritic cows. The drug was detected in milk for 36 h after administration. For MIC(90) of 0.5 microg.ml(-1) the most appropriate dosage for ceftriaxone, would be 9.0 mg.kg(-1) repeated at 6 h intervals for the treatment of endometritis in cows.

Alterations in electrocardiographic parameters after subacute exposure of fluoride and ameliorative action of aluminium sulphate in goats.

Fluorosis or crippling disease is one of the existing environmental challenges for animal and human beings in most parts of the globe. In the present study, sodium fluoride alone and with aluminium sulphate (ameliorative agent) was administered orally daily for 30 days in healthy goats of group 1 and 2, respectively, to access the effect on the electrocardiogram. All waves of Lead I, Lead II, Lead III, aVR, aVL and aVF in electrocardiographs were recorded before and after 30 days exposure of fluoride. A significant (P < 0.05) increase in P-R, Q-T and S-T intervals were observed in goats of group 1 as compared to their pre treatment values. The T wave duration was also significantly (P < 0.05) prolonged and as a result, bradycardia was observed after subacute exposure of fluoride for 30 days in group 1. But, in group 2, no such changes were observed. On the basis of results, it may be concluded that subacute toxicity of fluoride produces significant changes in different waves of electrocardiogram and aluminium sulphate has ameliorative efficacy.

Induction of oxidative stress and lipid peroxidation in rats chronically exposed to cypermethrin through dermal application.

Present study was undertaken to study the effect of cypermethrin on oxidative stress after chronic dermal application. The insecticide was applied dermally at 50 mg/kg body weight in different groups of Wistar rats of either sex weighing 150-200 g. Significant (p < 0.05) increase in catalase activity was observed after 30 days of exposure. However, the superoxide dismutase activity declined significantly after 60 days of exposure. The activity of glutathione peroxidase and blood glutathione levels declined significantly (p < 0.05) after 30 days of cypermethrin dermal application. However, the activity of glutathione S-transferase increased significantly (p < 0.05) in all groups after 60 days of dermal exposure. Significant increase in lipid peroxidation was observed from 30 days onwards and reached a peak after 120 days of application.