Skip to main content
NCBI home page
Toxicology Research logoLink to Toxicology Research
. 2022 Dec 18;12(1):33–38. doi: 10.1093/toxres/tfac080

Glutathione attenuated lambda-cyhalothrin-induced alteration of serum total cholesterol concentration and oxidative stress parameters in rats

Akande Motunrayo Ganiyat 1,✉, Ogunnubi Johnson Caleb 2, Akumka David Dezi 3, Mohammed Adamu 4
PMCID: PMC9972829  PMID: 36866217

Abstract

Background

Lambda-cyhalothrin is a type II pyrethroid insecticide that is used for pest control in agricultural, domestic, and industrial settings. Glutathione is an antioxidant that has been reported to confer protection on biological systems against the adverse impacts of insecticides.

Objective

The aim of the study was to evaluate the effects of glutathione on the serum lipid profile and oxidative stress parameters of rats exposed to lambda-cyhalothrin toxicity.

Methods

Thirty-five rats were assigned into 5 groups each. Distilled water was given to the first group, whereas the second group received soya oil (1 mL/kg). Lambda-cyhalothrin (25 mg/kg) was administered to the third group. The fourth group was given lambda-cyhalothrin (25 mg/kg) and glutathione (100 mg/kg) successively, whereas the fifth group received lambda-cyhalothrin (25 mg/kg) and glutathione (200 mg/kg) consecutively. The treatments were administered once daily by oral gavage for 21 days. The rats were sacrificed after the completion of the study. The serum lipid profile and oxidative stress parameters were assessed.

Results

A significant (P < 0.05) increase was observed in the total cholesterol concentration of the lambda-cyhalothrin group. The serum malondialdehyde level was elevated (P < 0.05) in the lambda-cyhalothrin group. The superoxide dismutase activity of the lambda-cyhalothrin+glutathione200 group was enhanced (P < 0.05). The results revealed that lambda-cyhalothrin perturbed the total cholesterol concentration of the rats, whereas glutathione (particularly at 200 mg/kg, indicating a dose–response effect) ameliorated the disruptive impacts of lambda-cyhalothrin.

Conclusion

The advantageous effects of glutathione may be ascribed to its antioxidant property.

Keywords: lambda-cyhalothrin, glutathione, serum lipid profile, subacute toxicity, oxidative stress

Graphical Abstract

Graphical Abstract.

Graphical Abstract

Open in a new tab

1. Introduction

Pesticides are chemical constituents that are specifically introduced into the environment for the elimination of pests, as well as the prevention of crop losses and vector-borne diseases.1 Lambda-cyhalothrin [α-cyano-3-phenoxybenzyl 3-(2-chloro-3,3,3-trifluoro-1-propenyl)-2,2-dimethylcyclopropanecarboxylate, LCT] belongs to the group of pesticides known as pyrethroid insecticides.2,3 LCT is a type II pyrethroid that contains the α-cyano moiety.4 Insecticide products that contain pyrethroids have been employed for the control of insect pests in agricultural practice, public health, homes, farms, and gardens.5

Pyrethroids are commonly applied in agricultural, domestic, and animal husbandry settings because of their apparent low mammalian toxicity, reduced environmental persistence, and selective insecticidal activity.6 Pyrethroids act primarily on the voltage-gated sodium channels in neurons thereby causing neurotoxic symptoms in target organisms.7 In addition, LCT evokes oxidative stress in biological systems thereby causing aberrations in different functions of living organisms.8–9 Oxidative stress refers to an imbalance between oxidants and antioxidants in favor of the former, thereby ensuing in an overall rise in cellular levels of reactive oxygen species (ROS).3 Consequently, damage of macromolecules including nucleic acids, lipids, and proteins occur, as well as changes in cell function.10 It is noteworthy that a low-to-modest level of ROS is indispensable for cellular function and survival.11

Glutathione (l-γ-glutamyl-l-cysteinyl-glycine, C10H17N3O6S, GSH) is an antioxidant produced in cells, and it contains the amino acids, glutamine, glycine, and cysteine.12 An antioxidant is a substance capable of inhibiting oxidative damage in molecules.13 GSH is a vital part of the biotransformation of xenobiotics, and it protects the body from reducing agents.14 Besides, GSH acts as a protective agent against insecticides,15 and it plays a role in the detoxification of different electrophilic compounds and peroxides through catalysis by glutathione S-transferase and glutathione peroxidase.16 GSH has also been reported to possess lipid-lowering effects due to its antioxidant activity.17

The purpose of this study was to find out if GSH could attenuate the effects of LCT on the serum lipid profile and oxidative stress indices of male Wistar rats.

2. Materials and methods

2.1 Experimental animals

The adult Wistar rats used in this research were obtained from the Department of Animal Production, Faculty of Veterinary Medicine, University of Nigeria, Nsukka, Enugu State, Nigeria. They weighed between 101 and 149 g. They were acclimatized for 2 weeks before the research started. They were housed in cages under standard environmental conditions (23–25 °C, 12 h light/dark cycle). In addition, they were given standard rat chow and water ad libitum. The experimentation, conveyance, and care of the animals were conducted in accordance with the guidelines of the National Institute of Health Guide for Care and Use of Laboratory animals.18

2.2 Chemicals

A commercial grade of LCT (Lara Force®) containing 100 mL of 100% solution was procured from an agrochemical company in Abuja, Nigeria. It was reconstituted as a 2.5% solution of LCT in soya oil (Grand Cereals and Oil Mills Limited, Jos, Nigeria) before it was given to the Wistar rats.

A pharmaceutical grade of GSH reduced (Chemical Abstract Service Number: 70-18-8; Jarrow Formulas) was obtained from a pharmaceutical store in Abuja, Nigeria. It was reconstituted daily in distilled water to yield a 100 mg/mL solution before administration to the rats.

2.3 Determination of the median lethal dose of lambda-cyhalothrin

The median lethal dose (LD50) of lambda-cyhalothrin (LCT) was determined according to.19 In the first phase, 9 male Wistar rats were divided into 3 groups (A, B, and C) of 3 animals each. The rats in group A were administered with LCT at 10 mg/kg orally by gavage, whereas those in groups B and C were administered with LCT at 100 mg/kg and 1,000 mg/kg orally, respectively. The animals were observed for death within 24 h.

The second phase of the test was conducted based on the results obtained in the first phase. It entailed the use of 4 rats, individually caged and labelled as A, B, C, and D each. The rats were administered with LCT at doses of 20, 40, 60, and 80 mg/kg, respectively.

The LD50 was calculated as the square root of the product of the highest dose that did not cause mortality (designated as D0) and that of the lowest dose that produced mortality (designated as D100). The LD50 of LCT was calculated as follows:

LD50 = √(D0 × D100).

2.4 Subacute toxicological study

The rats were weighed and assigned to 5 groups with 7 rats in each group. Distilled water was given to the DW group, whereas soya oil was administered to the SO group (1 mL/kg). The LCT group received lambda-cyhalothrin at 25 mg/kg (~0.5 LD50), whereas the LCT + GSH100 group was administered with lambda-cyhalothrin (25 mg/kg) and glutathione (100 mg/kg,20,21) consecutively. The LCT + GSH200 group was given LCT (25 mg/kg) and then glutathione (200 mg/kg,21,22) successively. The treatments were administered once daily by oral gavage for 3 weeks. The rats were observed for clinical signs of toxicity during the investigation. Their body weights were measured a week before the start of the study (week 0), and subsequently on a weekly basis (weeks 1–3). At the conclusion of the study, the rats were sacrificed and 3 mL of blood samples were collected into plain sample bottles.

2.5 Evaluation of the serum lipid profile

The serum lipid profile analyzed included total cholesterol (TC), triglycerides (TG), and high density lipoprotein (HDL). The parameters were assayed with an auto analyzer (Bayer Express plus, Bayer, Germany). The low density lipoprotein level (LDL), very low density lipoprotein (VLDL), and atherogenic index (AI) were calculated.

2.6 Calculations

The VLDL level was calculated using the following equation: VLDL (mg/dL) = 0.2 × TG,23 whereas the LDL was calculated as follows:

LDL (mg/dL) = TC − HDL − (0.2 × TG).23 The AI was calculated as follows24:

graphic file with name DmEquation66.gif

2.7 Determination of malondialdehyde concentration in the serum

The concentration of malondialdehyde (MDA) was evaluated in the serum by using an MDA assay kit (Elabscience Biotechnology Incorporation, Elabscience Texas, United States). The method described by Draper and Hadley25 was used. The principle of the method is based on the spectrophotometric measurement of the color produced during the reaction of thiobarbituric acid with MDA. The concentration of MDA in the samples was calculated by using the absorbance coefficient of MDA-thiobarbituric acid complex 1.56 × 105/cm/M. The MDA in the serum samples was expressed as nmol/mL.

2.8 Assessment of the activities of antioxidant enzymes in the serum samples

Superoxide dismutase (SOD) activity was evaluated in the serum samples with the SOD assay kit (Elabscience Biotechnology Incorporation, Elabscience Texas, United States). The principle of the method was based on autoxidation of haematoxylin.26 Catalase (CAT) activity was analyzed in the serum samples with the CAT assay kit (Elabscience Biotechnology Incorporation, Elabscience Texas, United States). The method used was based on the consumption of H2O2 substrate.27 The assays were conducted according to the manufacturer’s stipulations.

2.9 Statistical analysis

The data were expressed as mean ± standard error of the mean. The biochemical parameters were analyzed using 1-way analysis of variance, followed by Tukey’s multiple comparison post-hoc test. The statistical package used was GraphPad Prism version 4.00 for Windows (GraphPad software, California, United States). Values of P < 0.05 were considered statistically significant.

3. Results

3.1 Clinical observations

The rats in the group administered with LCT exhibited some signs of toxicity such as hypersalivation, muscle tremor, lethargy, and anorexia. The animals in the other groups did not manifest signs of toxicity.

3.2. Median lethal dose of lambda-cyhalothrin

In the first phase of the test, the rats exposed to LCT at 100 and 1,000 mg/kg all died, whereas the ones treated with LCT at 10 mg/kg survived. In the second phase of the test, the rats administered with LCT at 20 and 40 mg/kg, respectively survived, whereas those that were given LCT at 60 and 80 mg/kg, respectively died.

The highest dose that did not cause mortality was 40 mg/kg (designated as D0), whereas the lowest dose that produced mortality was 60 mg/kg (designated as D100).

The oral LD50 of LCT was calculated as 49 mg/kg.

3.3 Effects of the treatments on the body weights of the rats

The body weights of the experimental animals in all the groups increased progressively during the study (Fig. 1). The percentage alterations in the body weights of the rats at week 0 compared with week 3 were: DW (29%), SO (36%), LCT (23%), LCT + GSH100 (24%), and LCT + GSH200 (23%). There were no significant differences among the groups at weeks 0 and 1. However, at weeks 2 and 3, there were significant declines (P < 0.05) in the body weights of the rats in the LCT group compared with those in the LCT + GSH100 and LCT + GSH200 groups, respectively.

Fig. 1.

Fig. 1

Open in a new tab

Effects of the treatments on the body weights of the rats.

3.4 Impacts of the treatments on the serum lipid profile of the rats

There was a significant (P < 0.05) increase in the total cholesterol concentration of the LCT group (99.29 ± 3.06) compared with that of the DW group (86.99 ± 2.81) (Table 1).

Table 1.

Effects of the treatments on the serum lipid profile of Wistar rats.

Parameters (mg/dL) DW SO LCT LCT + GSH100 LCT + GSH200
Total cholesterol 86.99 ± 2.81 91.10 ± 3.95 99.29 ± 3.06 * 95.42 ± 3.14 94.52 ± 3.70
Triglycerides 66.84 ± 8.30 7.81 ± 9.85 80.36 ± 3.98 76.40 ± 2.87 74.90 ± 8.05
High density lipoprotein 51.28 ± 3.46 5.76 ± 2.38 50.34 ± 3.49 52.61 ± 2.08 54.46 ± 2.0
Very low density lipoprotein 13.37 ± 1.66 14.16 ± 1.97 16.07 ± .80 15.28 ± .57 14.98 ± 1.61
Low density lipoprotein 22.33 ± 3.87 26.18 ± 7.19 29.85 ± 3.76 28.91 ± 6.06 26.74 ± 2.16
Atherogenic index 0.72 ± 0.08 0.82 ± 0.06 0.92 ± 0.17 0.84 ± 0.10 0.82 ± 0.15
Open in a new tab

Distilled water: DW.

Soya oil: SO.

Lambda-cyhalothrin (25 mg/kg): LCT.

Lambda-cyhalothrin (25 mg/kg) + Glutathione (100 mg/kg): LCT + GSH100.

Lambda-cyhalothrin (25 mg/kg) + Glutathione (200 mg/kg): LCT + GSH200.

* P < 0.05 LCT group versus DW group.

3.5 Effects of the treatments on serum oxidative stress parameters

3.5.1 Effects of the treatments on serum malondialdehyde concentration

There was a significant (P < 0.05) upsurge in the serum MDA concentration of the group exposed to LCT compared with those of the DW, SO, and LCT + GSH200 groups, respectively (Fig. 2).

Fig. 2.

Fig. 2

Open in a new tab

Effects of the treatments on serum malondialdehyde concentration.

3.5.2 Effects of the treatments on serum superoxide dismutase activity

A significant (P < 0.05) enhancement of the serum SOD activity was recorded in the group exposed to LCT + GSH200 compared with those of the DW, SO, LCT, and LCT + GSH100 groups, respectively (Fig. 3).

Fig. 3.

Fig. 3

Open in a new tab

Effects of the treatments on serum superoxide dismutase activity.

3.5.3 Effects of the treatments on serum catalase activity

There was no remarkable difference (P > 0.05) in the CAT activity of the rats in the treatment groups (Fig. 4).

Fig. 4.

Fig. 4

Open in a new tab

Effects of the treatments on serum catalase activity.

4. Discussion

In the present study, the rats in the group administered with LCT exhibited some signs of toxicity such as hypersalivation, tremor, lethargy, and anorexia. The signs of toxicity were only observed after 1 h on the first day of administration. Tremor is a distinctive clinical sign triggered by exposure to pyrethroids.28,29 In a study conducted by Martínez et al.,3 transient tremor was only recorded daily during 2 h after pyrethroid administration. Subsequently, the behavior of the rats was similar to that of the control animals.

According to Verschoyle and Aldridge,30 poisoning with type II pyrethroids (e.g. LCT, cypermethrin, cyfluthrin, and deltamethrin) causes choreoathetosis-salivation (CS) syndrome entailing pawing and burrowing behavior, salivation, coarse tremor, progression to choreoathetosis, and clonic seizures. Type II pyrethroids also evoke sympathetic stimulation, skin paresthesia, and gastrointestinal irritation.31 The foregoing information may provide an explanation for the temporary toxic signs documented in the LCT group in this research.

In the current research, the oral LD50 of LCT was calculated as 49 mg/kg, and it may be classified as a highly hazardous substance.32 It has been affirmed that the oral LD50 of LCT is 79 and 56 mg/kg in male and female rats, respectively.33 Some investigators reported that the oral LD50 of LCT in male rats is 80 mg/kg,3,34 whereas Sharma et al.35 documented 60 mg/kg in male rats. The oral LD50 is not a biological constant and this might be the reason for the disparities in its value obtained in this investigation and those of other researchers.

In the present investigation, there were significant reductions in the body weights of the rats exposed to LCT at weeks 2 and 3 and this observation may be attributed to either decreased daily feed consumption or disorders in the levels of their metabolic hormones.36 Other investigators have also reported lowered body weights of rats exposed to LCT.37,38 However, exposure to LCT did not evoke any substantial effect on body weight gain in rats in some studies.3,39

Furthermore, LCT administered at 25 mg/kg induced a significant increase in the TC concentration of the male Wistar rats compared with the DW group. LCT is capable of increasing the level of TC in the serum, and this can occur through the excessive production of lipoproteins by the liver, reduced activity of receptors for LDL, and diminished affinity of circulating LDL for receptors.40 In contrast, the levels of the other indices comprising the serum lipid profile (TG, HDL, LDL, VLDL, and AI) were not different among the experimental groups. It has been reported that LCT elicited an elevation in the TC, TG, LDL, but a decrease in the HDL concentration of male rats in a study conducted by El-Saad and Abdel-Wahab.41 Similarly, Ghosh et al.42 documented that LCT caused an upsurge in serum TG, TC, LDL, and VLDL, but reduced serum HDL in female rats. The reasons for the differences between the results obtained in the present study and those of other researchers regarding the impacts of LCT on the serum lipid profile are unknown. However, the disparities observed may be ascribed to the formulations of LCT administered, duration and route of exposure, as well as the ages of the animals used.

It is noteworthy that GSH did not evoke significant ameliorative impacts on the serum lipid profile of the rats in this research. This finding is consistent with that of Akande et al.21 in which GSH did not exert profound attenuation of the adverse effects of lead acetate on the serum lipid profile of goats.

In the present investigation, the serum MDA level was significantly elevated in the group that was administered with LCT. This result is in agreement with those of other investigators.39,43 MDA is generated by the peroxidation of membrane polyunsaturated fatty acids, and the oxidation of MDA is regarded as a foremost indicator of lipid peroxidation.44 The finding in this study suggested that LCT can produce oxidative stress through the generation of free radicals by disruption of voltage-gated sodium channels in the axonal membrane, thereby engendering the alteration of the antioxidant system and perturbation of critical biomolecules in the rats.39

It was observed that the higher dosage of GSH (200 mg/kg) diminished the level of MDA. A dose-dependent effect was exerted by GSH in this regard. This outcome may be attributed to the antioxidant property of GSH.45 GSH evokes its antioxidant impacts by acting as a cofactor of numerous detoxifying enzymes; participating in amino acid transport; directly scavenging hydroxyl and singlet oxygen, as well as detoxifying hydrogen peroxide.46 Musthafa et al.47 stated that a substantial decline in GSH level in cells can cause a rise in the serum MDA concentration thereby resulting in oxidative stress.

There was a considerable improvement in the serum SOD activity in the LCT + GSH200 group relative to the other experimental groups. SOD is a metallo protein that scavenges superoxide radicals and changes them to hydrogen peroxide, thereby nullifying oxidative stress.48,49 The decline in the SOD activity in the LCT group in this research is in agreement with those of other researchers.50,51 Supplementation with GSH (200 mg/kg) brought about a more remarkable ameliorative impact on SOD activity compared with GSH administered at 100 mg/kg to the rats. This suggested a dose-dependent effect of GSH on the modulation of SOD activity in this research. GSH has been reported to augment SOD activity probably due to its antioxidant properties,46 and this is in accordance with the results obtained in this study.

There was no remarkable difference in the serum CAT activity among the groups. This finding negated the observations of other researchers who affirmed that LCT evoked a marked reduction of CAT activity in rats39 and aphids,43 whereas GSH caused a significant enhancement of CAT activity in rats.20 The underlying reasons for the differences in the results obtained regarding CAT activity in this research, and those of other investigators are unclear. It is surmised that the differences in the results may be attributable to the formulations of LCT applied, period and route of exposure, as well as the ages of the animals, among others.

5. Conclusion

It may be inferred from this study that LCT altered the total cholesterol concentration of the rats probably through the induction of oxidative stress. GSH might have demonstrated a dose-dependent attenuation of the disruptive effects of LCT through its antioxidant properties. There is a need for further studies to expound the mechanisms through which LCT evokes oxidative stress and perturbations in the serum lipid profiles of biological systems. In addition, the antioxidative mechanisms of GSH should be elucidated.

Authors’ contributions

MG and JC conceived the research and performed the experiment. JC, DD and A compiled the results. MG analyzed the results and wrote the manuscript. All the authors perused, revised and approved the final manuscript.

Acknowledgment

The authors are grateful to the staff of the Faculty of Veterinary Medicine, University of Abuja, Nigeria, for their support in the conduction of this research.

Contributor Information

Akande Motunrayo Ganiyat, Department of Veterinary Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Abuja, Federal Capital Territory, Abuja, 900001, Nigeria.

Ogunnubi Johnson Caleb, Department of Veterinary Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Abuja, Federal Capital Territory, Abuja, 900001, Nigeria.

Akumka David Dezi, Department of Veterinary Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Abuja, Federal Capital Territory, Abuja, 900001, Nigeria.

Mohammed Adamu, Department of Veterinary Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Abuja, Federal Capital Territory, Abuja, 900001, Nigeria.

Funding

The research was funded by the authors.

Conflict of interest statement: The authors affirm that there is no conflict of interest.

Declarations

Ethics approval: The experimental animals were treated in compliance with the guidelines of the National Institute of Health Guide for Care and Use of Laboratory animals,18 and with the approval of the University of Abuja Research Ethics Committee.

Consent to participate: This is not applicable for this research.

Consent for publication: This is not pertinent to this study.

Availability of data and materials: The data are included in the manuscript.

References

  • 1. Richardson JR, Fitsanakis V, Westerink RHS, Kanthasamy AG. Neurotoxicity of pesticides. Acta Neuropathol. 2019:138(3):343–362. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2. He LM, Troiano J, Wang A, Goh KS. Environmental chemistry, ecotoxicity, and fate of lambda-cyhalothrin. Rev Environ Contam Toxicol. 2008:195:71–91. [DOI] [PubMed] [Google Scholar]
  • 3. Martínez MA, Ares I, Rodríguez JL, Martínez M, Roura-Martínez D, Castellano V, Lopez-Torres B, Martínez-Larrañaga MR, Anadón A. Pyrethroid insecticide lambda-cyhalothrin induces hepatic cytochrome P450 enzymes, oxidative stress and apoptosis in rats. Sci Total Environ. 2018:631-632:1371–1382. [DOI] [PubMed] [Google Scholar]
  • 4. Lu Q, Sun Y, Ares I, Anadón A, Martínez M, Martínez-Larrañaga MR, Yuan Z, Wang X, Martínez MA. Deltamethrin toxicity: a review of oxidative stress and metabolism. Environ Res. 2019:170:260–281. [DOI] [PubMed] [Google Scholar]
  • 5. Amweg EL, Weston DP, Ureda NM. Use and toxicity of pyrethroid pesticides in the Central Valley, California, USA. Environ Toxicol Chem. 2005:24(4):966–972. [DOI] [PubMed] [Google Scholar]
  • 6. Gao Y, Sun Y, Jiang C, Yu X, Wang Y, Zhang H, Song D. Fast determination of pyrethroid pesticides in tobacco by GC-MS-SIM coupled with modified QuEChERS sample preparation procedure. Anal Sci. 2013:29(6):649–653. [DOI] [PubMed] [Google Scholar]
  • 7. Field LM, Davies TGE, O’Reilly AO, Williamson AO, Wallace BA. Voltage-gated sodium channels as targets for pyrethroid insecticides. Eur Biophys J. 2017:46(7):675–679. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8. Deeba F, Raza I, Muhammad N, Rahman H, Ur Rehman Z, Azizullah A, Khattak B, Ullah F, Daud MK. Chlorpyrifos and lambda cyhalothrin-induced oxidative stress in human erythrocytes. Toxicol Ind Health. 2016:33(4):297–307. [DOI] [PubMed] [Google Scholar]
  • 9. Aouey B, Derbali M, Chtourou Y, Bouchard M, Khabir A. Fetoui H, Pyrethroid insecticide lambda-cyhalothrin and its metabolites induce liver injury through the activation of oxidative stress and proinflammatory gene expression in rats following acute and subchronic exposure. Environ Sci Pollut Res Int. 2017:24:5841–5856. [DOI] [PubMed] [Google Scholar]
  • 10. Birben E, Sahiner UM, Sackesen C, Erzurum S, Kalayci O. Oxidative stress and antioxidant defense. World Allergy Org J. 2012:5:9–19. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11. Ahamed M, Akhtar MJ, Khan MAM, Alaizeri ZM, Alhadlaq H. Facile synthesis of Zn-doped Bi2O3 nanoparticles and their selective cytotoxicity toward cancer cells. ACS Omega. 2021a:6:17353–17361. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12. Lu SC. Glutathione synthesis. Biochim Biophys Acta. 2013:1830(5):3143–3153. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13. Abdollahi M, Ranjbar A, Shadnia S, Nikfar S, Rezaie A. Pesticides and oxidative stress: a review. Med Sci Monit. 2004:10(6):141–147PMID: 15173684. [PubMed] [Google Scholar]
  • 14. Seo JH, Pyo S, Shin YK, Nam BG, Kang JW, Kim KP, Lee HY, Cho SR. The effect of environmental enrichment on glutathione-mediated xenobiotic metabolism and antioxidation in normal adult mice. Front Neurol. 2018:9:425. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15. Eissa OS. Protective effect of vitamin C and glutathione against the histopathological changes induced by imidacloprid in the liver and testis of Japanese Quail. Egyptian J Hosp Med. 16:39–54. [Google Scholar]
  • 16. Anderson ME. Glutathione: an overview of biosynthesis and modulation. Chem Biol Interact. 1998:111:1–14. [DOI] [PubMed] [Google Scholar]
  • 17. Sudha M, Rajkumar D. Effect of glutathione in lipid profile in isoprenaline induced myocardial infarction in male albino rats. MedPulse Int. J Physiol. 2019:11(2):45–48. [Google Scholar]
  • 18. Garber JC, Barbee RW, Bielitzki JT, Clayton LA, Donovan JC, Kohn DF, Lipman NS, Locke P, Melcher J, Quimby FW, et al. Guide for the care and use of laboratory animals. 8th ed. Washington, DC: The National Academies Press; 2011. p. 246 [Google Scholar]
  • 19. Lorke D. A new approach to acute toxicity testing. Arch Toxicol. 1983:54(4):275–287. [DOI] [PubMed] [Google Scholar]
  • 20. Ahmadvand H, Babaeenezhad E, Nasri M, Jafaripour L, Khorramabadi RM. Glutathione ameliorates liver markers, oxidative stress and inflammatory indices in rats with renal ischemia reperfusion injury. J Renal Inj Prev. 2019:8(2):91–97. [Google Scholar]
  • 21. Akande MG, Wazehorbor JK, Chianumba FO, Okoronkwo SM. The ameliorative effects of glutathione on biochemical indices of goats exposed to lead. Japanese J Vet Res. 2020:68(4):217–225. [Google Scholar]
  • 22. Loguercio C, D'Argenio G, Delle Cave M, Cosenza V, Della Valle N, Mazzacca G, Del Vecchio BC. Glutathione supplementation improves oxidative damage in experimental colitis. Dig Liver Dis. 2003:35:635–641. [DOI] [PubMed] [Google Scholar]
  • 23. Friedewald WT, Levy RI, Fredickson DS. Estimation of the concentration of low density lipoprotein cholesterol in plasma without use of the preparative ultracentrifuge. Clin Chem. 1972:18(6):499–502PMID: 4337382. [PubMed] [Google Scholar]
  • 24. Lee RD, Nieman DC. Nutrition assessment. 6th ed. Boston: McGraw-Hill; 2012. ISBN: 9780078021336 0078021332 [Google Scholar]
  • 25. Draper HH, Hadley M. Malondialdehyde determination as index of lipid peroxidation. Methods Enzymol. 1990:186:421–431. [DOI] [PubMed] [Google Scholar]
  • 26. Martin JP Jr, Dailey M, Sugarman E. Negative and positive assays of superoxide dismutase based on haematoxylin autoxidation. Arch Biochem Biophys. 1987:255(2):329–336. [DOI] [PubMed] [Google Scholar]
  • 27. Beers RF, Sizer IW. A spectrophotometry method for measuring the breakdown of hydrogen peroxide by catalase. J Biol Chem. 1952:195(1):133–140PMID: 14938361. [PubMed] [Google Scholar]
  • 28. Soderlund DM, Clark JM, Sheets LP, Mullin LS, Piccirillo VJ, Sargent D, Stevens JT, Weiner ML. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. Toxicology. 2002:171(1):3–59. [DOI] [PubMed] [Google Scholar]
  • 29. U.S. Department of health and Human Services (USDHHS) . Toxicological profile for pyrethrins and pyrethroids. Atlanta, Georgia, USA: Agency for Toxic Substances and Disease Registry; 2003. https://www.atsdr.cdc.gov/toxprofiles/tp155.pdf. [PubMed]
  • 30. Verschoyle RD, Aldridge WN. Structure-activity relationships of some pyrethroids in rats. Arch Toxicol. 1980:45(4):325–329. [DOI] [PubMed] [Google Scholar]
  • 31. Ray DE, Forshaw PJ. Pyrethroid insecticides: poisoning syndromes, synergies, and therapy. J Toxicol Clin Toxicol. 2000:38(2):95–101. [DOI] [PubMed] [Google Scholar]
  • 32. WHO (World Health Organisation) . The WHO recommended classification of pesticides by hazard and guidelines to classification. Geneva, Switzerland: World Health Organization; 2019edition. ISBN: 9789240005662. 2022
  • 33. US EPA/HED (United States Environmental Protection Agency/Health Effects Division) . 2002. Cyhalothrin and lambda - 4th report of the hazard identification assessment review committee. Washington DC, USA: United States Environmental Protection Agency; https://www3.epa.gov/pesticides/chemical/foia/cleared-reviews/reviews/128897/128897-2002-09-12a.pdf.
  • 34. Ramadhas M, Palanisamy K, Sudhagar M, Mani VM. Ameliorating effect of Phoenix dactylifera on lambda cyhalothrin induced biochemical, hematological and hepatopathological alterations in male Wistar rats. Biomed Aging Pathol. 2014:4(3):273–279. [Google Scholar]
  • 35. Sharma DC, Saxena PN, Singh VK, Sharma R. Assessment of DNA degradation in lymphocytes of albino rat (Rattus norvegicus) under lambda cyhalothrin stress. World Appl Sci J. 2010:11(1):24–28. [Google Scholar]
  • 36. Ali A, Khan JA, Khaliq T, Javed I, Muhammad F, Aslam B, Khan MZ. Hemato-biochemical disruptions by lambdacyhalothrin in rats. Pak Vet J. 2014:34(1):54–57. [Google Scholar]
  • 37. El-Masry AA, Yousef MI, Hussein HK, Kheirallah NA, Straalen NM. L-carnitine protects against oxidative stress induced by sublethal exposure to the synthetic pyrethroid, lambdacyhalothrin, in rats. Glob Adv Res J. 2014:3(2):12–24. [Google Scholar]
  • 38. Al-Amoudi WM. Toxic effects of lambda-cyhalothrin, on the rat thyroid: involvement of oxidative stress and ameliorative effect of ginger extract. Toxicol Rep. 2018:5:728–736. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 39. Djahra AB, Benkaddour M, Benkherara S, Ouahiba B. Antioxidant and hepatoprotective potential of Coriandrum sativum L. against hepatic injury by lambda-cyhalothrin insecticide. J Drug Delivery Ther. 2020:10(3-s):182–188. [Google Scholar]
  • 40. Vega GL, Grundy SM. Mechanisms of primary hypercholesterolemia in humans. Am Heart J. 1987:113(2):493–502. [DOI] [PubMed] [Google Scholar]
  • 41. El-Saad AMA, Abdel-Wahab WM. Naringenin attenuates toxicity and oxidative stress induced by lambda-cyhalothrin in liver of male rats. Pak J Biol Sci. 2020:23(4):510–517. [DOI] [PubMed] [Google Scholar]
  • 42. Ghosh R, Das T, Paramanik A, Choudhury SM. Lambda cyhalothrin elicited dose response toxicity on haematological, hepatic, gonadal and lipid metabolic biomarkers in rat and possible modulatory role of taurine. Toxicol Forensic Med Open J. 2016:1(2):42–51. [Google Scholar]
  • 43. Dong B, Liu XY, Li B, Li MY, Li SG, Liu S. A heat shock protein protects against oxidative stress induced by lambda-cyhalothrin in the green peach aphid (Myzus persicae). Pestic Biochem Physiol. 2021:181:104995. [DOI] [PubMed] [Google Scholar]
  • 44. Delpech B. The saraine alkaloids. Alkaloids Chem Biol. 2014:73:223–329. [DOI] [PubMed] [Google Scholar]
  • 45. Korwa I, Muniroh M, Kristina T, Prasetyo A, Mahati E. Effect of glutathione administration as adjuvant therapy to NO and MDA level in Wistar rat peritonitis model. Bali Med J. 2021:10(2):713–716. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 46. Rocha M, Herance R, Rovira S, Hernandez-Mijares A, Victor VM. Mitochondrial dysfunction and antioxidant therapy in sepsis. Infect Disord Drug Targets. 2012:12(2):161–178. [DOI] [PubMed] [Google Scholar]
  • 47. Musthafa QA, Abdul Shukor MF, Ismail NAS, Mohd Ghazi A, Mohd Ali R, Nor IFM, Dimon MZ, Wan Ngah WZ. Oxidative status and reduced glutathione levels in premature coronary artery disease and coronary artery disease. Free Radic Res. 2017:51(9–10):787–798. [DOI] [PubMed] [Google Scholar]
  • 48. Younus H. Therapeutic potentials of superoxide dismutase. Int J Health Sci. 2018:12(3):88–93PMID: 29896077. [PMC free article] [PubMed] [Google Scholar]
  • 49. Ahamed M, Akhtar MJ, Khan MAM, Alhadlaq HA. SnO2-doped ZnO/reduced graphene oxide nanocomposites: synthesis, characterization, and improved anticancer activity via oxidative stress pathway. Int J Nanomedicine. 2021b:16:89–104. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 50. Fetoui H, Makni M, Mouldi Garoui E, Zeghal N. Toxic effects of lambda-cyhalothrin, a synthetic pyrethroid pesticide, on the rat kidney: involvement of oxidative stress and protective role of ascorbic acid. Exp Toxicol Pathol. 2010:62(6):593–599. [DOI] [PubMed] [Google Scholar]
  • 51. Abdellatif AM, Nasr HM, Mansy AS. Rutin and vitamin E alleviate oxidative stress and hepatic-renal injury induced by technical and formulated lambda-cyhalothrin in adult rats. GSC Biol Pharmaceut Sci. 2020:12(1):31–40. [Google Scholar]

Articles from Toxicology Research are provided here courtesy of Oxford University Press

RESOURCES