Neurotoxicity of dichlorvos: Effect on antioxidant defense system in the rat central nervous system

Julka, Deepinder; Pal, Ravinder; Gill, Kiran Dip

doi:10.1016/0014-4800(92)90031-6

Cited by 52 publications

(20 citation statements)

References 20 publications

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“…The oxygen radicals that are normally produced within the body are usually kept in check by complex multifactorial protective enzymes, which include the superoxide dismustase, catalases, and glutathione peroxidase, which can check the free radicals originating either in the mitochondria or in the cytoplasm. However, the brain is one organ that is, at first instance, susceptible to peroxidase damage because of several factors, such as high oxygen tension, low mitotic rate, high lipid content, and as well as low antioxidant concentration [25]. These factors perhaps explain why lead exposure affects brain more than any other organ.…”

Section: Discussionmentioning

confidence: 99%

Lead intoxication: Histological and oxidative damage in rat cerebrum and cerebellum

Sidhu¹,

Nehru²

2004

J Trace Elements Exper Med

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The present experiment was designed to study the neurotoxic consequences of lead exposure on antioxidant enzymes like glutathione, glutathione peroxidase, super oxide dismustase, and catalase along with structural changes both in cerebrum as well as cerebellum. Lead was administrated orally in the doses of 50 mg/kg for a period of 8 weeks and study was performed at the end of exposure. Decrease in the concentration of all the antioxidant enzymes was observed, and after lead treatment, transverse sections of cerebrum showed degeneration of neurons. Disruption of normal arrangement of cell layers was seen. Cells were bigger in size with large vascular spaces around them. Lead treatment for 8 weeks also was enough to disrupt the normal arrangement of cellular layer of cerebellum. Large spaces in between purkinje cell layer and granular layer were seen.

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Section: Discussionmentioning

confidence: 99%

Lead intoxication: Histological and oxidative damage in rat cerebrum and cerebellum

Sidhu¹,

Nehru²

2004

J Trace Elements Exper Med

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“…The oxygen radicals that are normally produced within the body are usually kept in check by complex multifactorial protective enzymes, which include catalase, superoxide dismutase and glutathione peroxidase, which can check the free radicals originating either in the mitochondria or in the cytoplasm. However, the brain is one organ that is, at first instance, susceptible to peroxidase damage ( Julka et al, 1992). Lead can alter the cellular redox state by inhibiting the enzymes involved in antioxidant defense, that is catalase, glutathione peroxide, glutathione and superoxide dismutase, which function as blockers of free radical process (Dormandy, 1978).…”

Section: Discussionmentioning

confidence: 99%

Lead Toxicity and The Hypothalamic-Pituitary-Testicular Axis

Hamadouche¹,

Nesrine²,

Abdelkeder³

2013

Not Sci Biol

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Environmental exposure to toxic levels of lead (Pb) occurs in a number of industries with potential adverse effects on the reproductive capacity of exposed men. Clinical and animal studies indicate that abnormalities of spermatogenesis result from toxic lead exposure, but eventual histopathologic alterations involved have not been identified. To explore putative abnormalities in the reproductive gonadotropic axis following lead intoxication, experimental animals when exposed to low levels of lead, 65 days old animals were treated with distilled water containing 0,0 mg (control), 10 mg lead (Pb)/Kg/day and 15 mg lead (Pb)/Kg/day intraperitoneally for 20 days. At the end of treatment, the animals were sacrificed and the blood collected for luteinizing hormone (LH) and testosterone assays. The testis was processed for histological analysis. The results showed a high serum concentration of LH and testosterone in lead-treated animals compared to controls. Histological examination of testis showed deformities in testicular morphology of lead intoxicated animals with gross damage within the somniferous tubules. A strong correlation was established between LH and testosterone suggesting an alteration in the endocrine components of the gonadotropic axis. Histological examination of pituitary gland showed some degenerative changes in endocrine cells of lead group. Changes in LH and testosterone levels suggest that Pb exposure during the critical time of sexual differentiation induces reproductive axis abnormalities in adulthood. In conclusion, lead has a gonadotoxic effect by decreasing LH and testosterone levels and damaging the testis seminiferous tubules. Catalase activity was significantly reduced in the lead group following 65 days of exposure which possibly indicates that lead might had other mechanisms of action, such as increasing oxidative damage.

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“…Studies have revealed that phosphamidon, trichlorfon, and dichlorvos pesticides induce oxidative stress, as shown by enhanced superoxide dismutase (SOD) activity, lipid peroxidation, and a decrease in glutathione peroxidase activity (Julka et al, 1992). Similarly, intoxication of the organophosphate bidrin has also been shown to induce the formation of ROS and thus induce renal tubular epithelial cell toxicity (Poovala et al, 1999).…”

Section: Pesticide-induced Dna Damage and Oxidative Stressmentioning

confidence: 99%

“…This cascade includes (in part but not limited to) the production of reactive oxygen species (ROS) and oxidative stress from increased lipid peroxidation (Stohs, 1990;Stohs et al, 1997), DNA single-strand breaks, doublestrand breaks and fragmentation (Bagchi et al, 1993;Hreljac et al, 2008;Muniz et al, 2008), apoptosis (Stohs, 1990;Stohs et al, 1997), glutathione depletion (Julka et al, 1992;Muniz et al, 2008), activation of protein kinase C Anticholinesterase Pesticides: Metabolism, Neurotoxicity, and Epidemiology. Edited by Tetsuo Satoh and Ramesh C. Gupta Copyright # 2010 John Wiley & Sons, Inc. (Bagchi et al, 1995Stohs, 1990), enhanced release of tumor necrosis factor-a (Stohs, 1990;Stohs et al, 1997), induction of stress/heat shock protein 90, stimulation of oncogene expression, and inhibition of tumor suppressor genes (Amundson et al, 1998;Bagchi et al, 2000).…”

Section: Introductionmentioning

confidence: 99%