Toxicology International (Formerly Indian Journal of Toxicology)

Poonam Sharma , Rambir Singh , Mysra Jan

Abstract

Objectives: Deltamethrin is a synthetic pyrethroid insecticide used worldwide in agriculture, household pest control, protection of foodstuff, and disease vector control. Although initially thought to be least toxic, a number of recent reports showed its toxic effects in mammalian and non‑mammalian animal species. The current study was performed to assess the dose‑dependent deltamethrin toxicity on testes, liver, and kidney of male Wistar rats. Materials and Methods: Twenty‑four rats were divided in four groups of 6 each. Group A served as normal control. Group B, C, and D were administered with different doses (2 or 3 or 6 mg/kg corresponding to 1/30th or 1/20th or 1/10th of LD50, respectively) of deltamethrin for 28 days. Results: Deltamethrin exposure caused a significant reduction in weight of reproductive organs, decrease in sperm count, sperm motility, serum testosterone (T), follicle stimulating hormones (FSH), and luteinizing hormones (LH) in testis. Glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione S transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPx) were decreased in testis, liver and kidney of exposed rats. Deltamethrin exposure significantly increased sperm abnormalities in testis. Significant increase in lipid peroxidation (LPO) level was observed in testis, liver and kidney. Deltamethrin also caused histological alterations in testes, liver, and kidney. Conclusions: The results indicated that deltamethrin at a dose of 6 mg/kg exerts significant harmful effects on testes, liver and kidney as compare to 2 mg and 3 mg/kg. The study concluded that the system toxicity induced by deltamethrin was dose dependent.

Keywords

Deltamethrin, kidney, liver, oxidative stress, testes, Wistar rats

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Poonam Sharma , Rambir Singh

Abstract

Trichlorfon is an organophosphate insecticide used to control cockroaches, crickets, silverfish, bedbugs, fleas, cattle grubs, flies, ticks, leaf miners, and leaf-hoppers. It is also used to treat domestic animals for control of internal parasites. Trans-2-hydroxycinnamic acid (T2HCA) is a hydroxyl derivative of cinnamic acid. The present study highlights trichlorofon-induced toxicity and the protective role of T2HCA in the liver, kidney, and brain of female Wistar rats. The rats were given a single dose of trichlorofon (150 mg / kg bw) and pre- and post-treatment T2HCA (50 mg / kg bw) for seven days. Trichlorofon enhanced oxidative stress in liver, kidney, and brain of the rats, which was evident from the elevation of lipid peroxidation (LPO). The reduced level of non-enzymatic antioxidant glutathione (GSH) also indicated the presence of an oxidative insult. The activity of enzymatic antioxidants like superoxide dismutase (SOD), catalase (CAT), glutathione-s-transferase (GST), glutathione reductase (GR), and glutathione peroxidase (GPx) was significantly decreased on trichlorfon administration. Pre and post treatment with T2HCA decreased the LPO level and increased SOD, CAT, GST, GR, GPx, and GSH in the brain, liver, and kidney. Trichlorfon-induced reduction in acelylcholinestrase was also ameliorated with T2HCA treatment. In conclusion, trichlorfon-mediated induction in the reactive oxygen species and disturbance in the antioxidant enzymes’ defense system was moderately ameliorated by antioxidant trans-2-hydroxycinnamic acid.

Keywords

Oxidative stress, trans-2-hydroxycinnamic acid, trichlorfon, Wistar rats

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Rambir Singh ¹, Poonam Sharma ¹

Affiliations
1 Departments of Biomedical Sciences and Zoology, Bundelkhand University, Jhansi, Uttar Pradesh, IN

Abstract

Lindane, an organochlorine pesticide, is recognized as a major public health concern because of its potential toxic effects on human health. Its persistence in the body fluids may lead to continuous blood circulation, liver exposure and hepatotoxicity. The present study was undertaken to evaluate the possible protective role of curcumin on lindane-induced hepatotoxicity. Forty-two healthy adult male Wistar rats were divided into seven groups of six rats each. Group I was given dimethylsulfoxide. A single dose of lindane (60 mg/kg bw) was given to group II. Lindane (30 mg/kg bw) was given daily to group III for 14 days. Treatment with curcumin (100 and 200 mg/kg) was given to groups IV and V before (pretreatment) and to groups VI and VII after (post-treatment) 14 days exposure of lindane. Oxidative stress parameters and antioxidative enzymes were investigated in the liver of exposed and treated rats. A significant increase in lipid peroxidation, and decrease in glutathione level, Superoxide dismutase catalase, glutathione-S-transferase, glutathione peroxidase, glutathione reductase and NADPH quinine reductase activities was observed in liver of rats exposed to lindane. Curcumin (Pre- and post-treatment) nearly normalized all these parameters. Histological alterations were also observed in the liver tissue after lindane exposure. Treatment with curcumin significantly prevented the lindane-induced histological alterations. In conclusion, curcumin has protective effect over lindane-induced oxidative damage in rat liver.

Keywords

Curcumin, hepatotoxicity, lindane, Wistar rat

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Vikas Pankaj Bhargava ¹, Aashish Kumar Netam ², Rambir Singh ³, Poonam Sharma ²

Affiliations
1 Department of Zoology, Indira Gandhi National Tribal University, Amarkantak - 484887, Madhya Pradesh, India; pnm245@yahoo.com, IN
2 Department of Zoology, Indira Gandhi National Tribal University, Amarkantak - 484887, Madhya Pradesh, IN
3 Department of Horticulture, Aromatic and Medicinal Plants, Mizoram University, Aizawl - 796004, Mizoram, IN

Abstract

Background and Aim: Exposure to Aluminium (Al) has been reported to cause neurotoxicity in laboratory animals. Amyloid-β (Aβ) plaque formation, tau protein hyperphosphorylation, and neuroinflammation have been indicated as the possible mechanism of Al-induced neurodegeneration. The present study aimed to understand the mechanism of aluminium chloride (AlCl3)-induced neurotoxicity in Wistar rats and to assess the neuroprotective effect of methanolic extract of Cassia tora leaves (MECT). Material and Methods: Seventy-two male Wistar rats were randomly divided into nine groups. AlCl3 (100 mg/kg bw) and MECT (300 mg/kg bw) were given orally by gavage and memantine (MEM) was administered intraperitoneally (20 mg/kg bw) to rats, daily for 60 days. The spatial learning memory and recognition memory were evaluated using the Morris Water Maze (MWM) test. The levels of oxidative stress, neurotransmitter markers, pro-inflammatory markers, Aβ proteins plaques formation and tau protein hyperphosphorylation were evaluated. Histopathology of brain tissue was performed to assess the extent of tissue damage on AlCl3 exposure. Results: MECT significantly improved cognitive behaviours in AlCl3-exposed rats during the MWM test. Treatment with MECT resulted in a significant recovery of antioxidant enzyme function, the activity of neurotransmitter markers and pro-inflammatory cytokine levels. MECT prevented the aggregation of Aβ proteins and tau protein phosphorylation. Also, it inhibited the loss of neuronal integrity in the cortex and hippocampus regions of the brain in AlCl3-exposed rats. Conclusion: The findings demonstrate that a methanolic extract of Cassia tora leaves ameliorated AlCl3-induced neurodegeneration in Wistar rats.

Keywords

Aluminium Chloride, Beta-amyloid, Cassia tora, Neurotoxicity, Tau Protein.

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