Papel del selenio sobre la capacidad antioxidante en ratones tratados con metomil

El-Khawaga, Omali Y.

doi:10.1007/bf03168375

Cited by 23 publications

(19 citation statements)

References 17 publications

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“…Recently Mahagoub and Medany [10] reported that chronic exposure of methomyl (17 mg/ kg body wt) for 2 months revealed significantly decreased SDH activity in rat testis. In the present study increase in LDH activity indicates leakage of LDH from tissues due to loss of membrane permeability caused by increased oxidative damage [56,57] or by depletion of ATP [58,59]. In the present study it has been found that increase in the dose and duration of exposure of methomyl caused decrease in the activity of Na + -k + ATPase, Mg ++ ATPase, and Ca ++ ATPase in the testes and epididymis.…”

Section: Discussionsupporting

confidence: 55%

Methomyl induced gonadal dysfunction, biochemical contents and enzyme activities in male albino mice

Bb¹,

Si²

2010

Int J of Biot Appl

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Abstract-Methomyl (S-methyl-1-N [(methyl carbamoyl) oxy] thio acetimidate, is a carbamate broad spectrum insecticide. The Swiss albino mice were administered orally 1, 2, 3, and 4 mg/kg body wt methomyl for 30 days and effective dose 4 mg/kg for 5, 10, and 20 days to know the dose and durational effect on testes and biochemical contents. The mice were sacrificed on day 31 st or 24 hours after the terminal exposure. Testes, epididymis, vasa deferentia, seminal vesicles, prostate, coagulatory and Cowper's glands weight decreased significantly with 2, 3 and 4 mg/kg/day and in 4mg/kg /day for 10 and 20 days of methomyl treatment.Histologic studies of the testes revealed anti-spermatogenic and anti-steroidogenic effects of methomyl reflected by significant decrease in the number and diameter of spermatogonia, primary spematocytes, secondary spermatocytes, spermatids and Leydig cells in the mice treated with 2, 3 and 4 mg/kg/day and in 4 mg/kg /day for 10 and 20 days of methomyl treatment, except with 2 mg/kg/day methomyl treatment number of primary spematocytes, Leydig cells, diameter of spermatogonia, and in 4 mg/kg/day methomyl for 10 days treatment the number of spermatogonia, leydig cells and diameter of primary spermatocytes not changed significantly when compared with controls. Biochemical studies of testis and epididymis showed methomyl at doses of 2, 3 and 4 mg/kg/day and in 4 mg/kg /day for 10 and 20 days of methomyl treatment caused significant decrease in the levels of DNA, RNA, protein, glycogen and sialic acid whereas cholesterol increased significantly. However, treatment with 1, 2 mg / kg/ day and 4 mg / kg /day for 5 days methomyl caused no significant change in epididymal biochemical contents when compared with control. Study on enzyme activities in testis and epididymis revealed that the treatment with 3 and 4 mg/kg/day and 4 mg/kg /day for 20 days of methomyl caused significant decrease in the activities of succinic dehydrogenase (SDH), ions ATPase (Na + -K + ATPase, Ca ++ ATPase, Mg ++ ATPase) and acid phosphatase (ACP) were decreased significantly, except with 3 mg/kg/day methomyl treatment where Ca ++ ATPase activity in testes and epididymis not changed significantly. However, lactate dehydrogenase (LDH) and alkaline phosphatase (AKP) activities were increased significantly. The testis 3β hydroxysteroid dehydrogenase (3βHSD) decreased significantly with 3 and 4 mg/kg /day and in 4 mg/kg /day for 10 and 20 days of methomyl treatment when compared with controls. However, there was no significant change in testes and accessory reproductive organs, number and diameter of spermatogonia and Leydig cells and biochemical contents of testis and epididymis with 1 mg/kg/day and in 4 mg/kg /day for 5 days of methomyl treatment. These observed effects of methomyl on testes and accessory reproductive organs weight, testis histology, biochemical contents and enzyme activities in testis and epididymis may be due to toxic effect or hormonal imbalance in any of the stage in the hypothalamo-hypophysial-testicular ...

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Section: Discussionsupporting

confidence: 55%

Methomyl induced gonadal dysfunction, biochemical contents and enzyme activities in male albino mice

Bb¹,

Si²

2010

Int J of Biot Appl

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“…The elevated LDH activity might be due to its leakage in the seminiferous tubular fluid from the germ cells which are damaged by the increased oxidative stress. [ 27 28 ] The increase in the ALP activity may also be attributed to the cellular leakage caused by chemical-induced injury of the tissue. [ 29 ]…”

Section: Discussionmentioning

confidence: 99%

Tribulus terrestris ameliorates metronidazole-induced spermatogenic inhibition and testicular oxidative stress in the laboratory mouse

Kumari

Singh

2015

Indian J Pharmacol

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Objective:The present study was undertaken to evaluate the protective effects of the fruit extract of Tribulus terrestris (TT) on the metronidazole (MTZ)-induced alterations in spermatogenesis, sperm count, testicular functions, and oxidative stress.Materials and Methods:Thirty adult Swiss strain mice were divided into six groups. Animals of Groups I and II served as untreated and vehicle-treated controls, while that of Groups III and IV were administered with MTZ (500 mg/kg BW/day) and TT (200 mg/kg BW/day) alone for 28 days, respectively. Low (100 mg/kg BW/day) and high (200 mg/kg BW/day) doses of TT along with MTZ (500 mg/kg BW/day) were administered for 28 days in the mice of Groups V and VI, respectively. Twenty four hours after the last treatment, all the animals were euthanized to study the histological changes in the testis and sperm count in the epididymis. Testicular functional markers, lipid peroxidation (LPO) and the activities of antioxidant enzymes, e.g., superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase, were also assessed in the mice of all the groups.Results:Metronidazole caused marked alterations in the testicular weight, spermatogenesis, activities of antioxidant enzymes, lactate dehydrogenase, alkaline phosphatase, and the level of LPO. The epididymal sperm count also declined significantly in MTZ-treated group. These changes were partially restored following co-administration of 500 mg/kg BW/day of MTZ and 100 mg/kg BW/day of TT. However, in the mice co-administered with 500 mg/kg BW/day of MTZ and 200 mg/kg BW/day of TT, the changes reverted back completely, similar to that of the controls.Conclusion:The fruit extract of TT ameliorates the MTZ-induced alterations in the testis.

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“…Upon postischemic GSH treatment, intravital fluorescence microscopy has demonstrated an almost complete restoration of sinusoidal blood flow, paralleled by a reduction of inflammatory leukocyte adherence in sinusoids and postsinusoidal venules, resulting in reduced necrotic tissue injury and improved rat survival (706). Micronutrients like selenium are observed to enhance the endogenous antioxidant capacity of the cells by increasing the activity of SOD and the GSH content (177). Accordingly, selenite supplementation significantly improves postischemic hepatic microcirculation by acting as a radical scavenger and by preserving the antioxidative capacity of the liver (949).…”

Section: A Antioxidative Antiadhesive and Anti-inflammatory Approamentioning

confidence: 96%

The Hepatic Microcirculation: Mechanistic Contributions and Therapeutic Targets in Liver Injury and Repair

Vollmar

Menger²

2009

Physiological Reviews

426

368

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The complex functions of the liver in biosynthesis, metabolism, clearance, and host defense are tightly dependent on an adequate microcirculation. To guarantee hepatic homeostasis, this requires not only a sufficient nutritive perfusion and oxygen supply, but also a balanced vasomotor control and an appropriate cell-cell communication. Deteriorations of the hepatic homeostasis, as observed in ischemia/reperfusion, cold preservation and transplantation, septic organ failure, and hepatic resection-induced hyperperfusion, are associated with a high morbidity and mortality. During the last two decades, experimental studies have demonstrated that microcirculatory disorders are determinants for organ failure in these disease states. Disorders include 1) a dysregulation of the vasomotor control with a deterioration of the endothelin-nitric oxide balance, an arterial and sinusoidal constriction, and a shutdown of the microcirculation as well as 2) an overwhelming inflammatory response with microvascular leukocyte accumulation, platelet adherence, and Kupffer cell activation. Within the sequelae of events, proinflammatory mediators, such as reactive oxygen species and tumor necrosis factor-alpha, are the key players, causing the microvascular dysfunction and perfusion failure. This review covers the morphological and functional characterization of the hepatic microcirculation, the mechanistic contributions in surgical disease states, and the therapeutic targets to attenuate tissue injury and organ dysfunction. It also indicates future directions to translate the knowledge achieved from experimental studies into clinical practice. By this, the use of the recently introduced techniques to monitor the hepatic microcirculation in humans, such as near-infrared spectroscopy or orthogonal polarized spectral imaging, may allow an early initiation of treatment, which should benefit the final outcome of these critically ill patients.

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Papel del selenio sobre la capacidad antioxidante en ratones tratados con metomil

Cited by 23 publications

References 17 publications

Methomyl induced gonadal dysfunction, biochemical contents and enzyme activities in male albino mice

Methomyl induced gonadal dysfunction, biochemical contents and enzyme activities in male albino mice

Tribulus terrestris ameliorates metronidazole-induced spermatogenic inhibition and testicular oxidative stress in the laboratory mouse

The Hepatic Microcirculation: Mechanistic Contributions and Therapeutic Targets in Liver Injury and Repair

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