Endocrine-disrupting and cytotoxic potential of anticholinesterase insecticide, diazinon in reproductive toxicity of male mice

ElMazoudy, Reda H.; Attia, Azza A.

doi:10.1016/j.jhazmat.2011.12.073

Cited by 31 publications

(22 citation statements)

References 53 publications

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“…Diazinon, an organophosphrus insecticide, has been widely used in industrial, veterinary, and agriculture practice, that would be potentially an exposure risk to animals and human as well (Larkin and Tjeerdema 2000). Although several investigations about DZN toxicity have been published, little study has been performed about the preventive agents used against such a toxicity and mechanism of their ameliorative action (Larkin and Tjeerdema 2000;Al-Attar and Abu Zeid 2013;Razavi et al 2013;Elmazoudy et al 2011;ElMazoudy and Attia 2012). In the present study, the renal injuries caused by DZN may be caused by the oxidative stress resulted from free radical production.…”

Section: Discussionmentioning

confidence: 65%

“…Moreover, it disrupts mitochondrial membrane transport in rat liver and affects cytochrome P450 system in human liver (Sams et al 2004). Furthermore, DZN toxicity induced oxidative damage resulting in hematological disorders, cardiotoxicity, hepatotoxicity, nephrotoxicity, neurotoxicity, and both female and male reproductive toxicity (AlAttar and Abu Zeid 2013; Razavi et al 2013;Elmazoudy et al 2011;ElMazoudy and Attia 2012).…”

Section: Introductionmentioning

confidence: 99%

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Synergistic protective role of ceftriaxone and ascorbic acid against subacute diazinon-induced nephrotoxicity in rats

Abdel-Daim

2014

Cytotechnology

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Diazinon (DZN) is a synthetic organophosphrus acaricide and insecticide widely used for veterinary and agricultural purposes. However, its animal and human exposure leads to nephrotoxicity. Our experimental objective was to evaluate protective effects of ceftriaxone and/or ascorbic acid-vitamin C against DZN-induced renal injury in male Wistar albino rats. DZN-treated animals revealed significant elevation in serum biochemical parameters related to renal injury: urea, uric acid and creatinine. DZN intoxication significantly increased renal lipid peroxidation, and significant inhibition in antioxidant biomarkers including, reduced glutathione, glutathione peroxidase, superoxide dismutase, catalase and total antioxidant capacity. In addition, DZN significantly reduced serum acetylcholinestrase level. Moreover, It induced serum and kidney tumor necrosis factor-a level. Both ceftriaxone and vitamin C protect against DZN-induced serum as well as renal tissue biochemical parameters when used alone or in combination along with DZN-intoxication. Furthermore, both ceftriaxone and vitamin C produced synergetic nephroprotective and antioxidant effects. Therefore, it could be concluded that ceftriaxone and/or vitamin C administration are able to minimize the toxic effects of DZN by its free radical-scavenging and potent antioxidant activity.

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Section: Discussionmentioning

confidence: 65%

Section: Introductionmentioning

confidence: 99%

Synergistic protective role of ceftriaxone and ascorbic acid against subacute diazinon-induced nephrotoxicity in rats

Abdel-Daim

2014

Cytotechnology

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“…Spermatozoa were collected and processed as described earlier in El‐Mazoudy & Attia (2012) 24 . Briefly, for sperm DNA condensation, dried sperm smears were fixed with 3% buffered glutaraldehyde in 0.2 M phosphate buffer (pH 7.2) for 30 minutes at room temperature.…”

Section: Methodsmentioning

confidence: 99%

Impact of vitamin D deficiency on mouse sperm structure and function

et al. 2020

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Background In rodents and humans, vitamin D deficiency (VDD) is associated with altered sperm structure and function (primarily decreased motility and morphological abnormalities) that are primarily attributed to VDD‐induced hypocalcemia. However, it is suspected that VDD has much more drastic effects on mammalian spermatozoa. Objectives The purpose of this study was to illustrate that VDD, depending on its severity and duration, can alter sperm nuclear integrity and can also lead to the loss of spermatozoa's ability to support embryonic development. Materials and methods A mouse model of induced VDD combining the action of a vitamin D‐deficient diet, UV exposure limitation, and paricalcitol injections; a vitamin D2 analog that catabolizes endogenous vitamin D by increasing the expression of CYP24A, a member of the cytochrome P450 family, has been used to create different grades of VDD. Results We show that the most significant sperm defect recorded concerns the integrity of the paternal nucleus, which is both decondensed and fragmented in moderate‐to‐severe VDD situations. Consistent with the known consequences of fertilization with DNA‐damaged spermatozoa, we show that paternal VDD decreases the ability of spermatozoa to optimally support fertilization and embryonic development. Discussion and Conclusion Given the worldwide high prevalence of VDD in humans, and although obtained in an animal model, the data presented here suggest that subfertile/infertile males may benefit from VDD testing and that attempts to correct serum vitamin D levels could be considered prior to conception, either naturally or through ART.

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“…Malathion or O,O‐dimethyl‐S‐1,2‐bis ethoxycarbonyl ethyl phosphorodithioate, a wide spectrum organophosphate insecticides used to kill agricultural fleas, is a neurotoxin that inhibits acetyl‐cholinesterase at synaptic junction, thereby inhibiting the hydrolysis of body choline esters (Cabello et al, ). Although malathion is a potential hazardous compound affecting mice, reptiles, birds, earthworms, and insects (Huculeci et al, ), minimal apprehension is available about its chronic and sublethal effects on the reproduction, specially of mammals (Espinoza‐Navarro and Bustos‐Obregon, ; El‐Mazoudy and Attia, ).…”

Section: Introductionmentioning

confidence: 99%

Granulosa cell apoptosis by impairing antioxidant defense system and cellular integrity in caprine antral follicles post malathion exposure

Bhardwaj

Saraf

2015

Environ. Toxicol.

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Toxicological studies have demonstrated the exposure-risk relationship of several pesticides on reproduction of living organisms. To evaluate the role of malathion as a reproductive toxicant, this study aims at assessing the cytological and biochemical changes in the granulosa cells after malathion exposure in dose (1 nM, 10 nM, 100 nM) and time (4 h, 6 h, 8 h) dependent manner. Histomorphological analysis, fluorescence assay, apoptosis quantification, and terminal deoxynucleotidyl transferase d-UTP mediated nick end labeling (TUNEL) assay were done to determine cytological changes, whereas antioxidant enzyme assays were done to measure the oxidative stress in malathion treated ovarian antral follicles. Histological studies exhibited the occurrence of highly condensed or marginated chromatin with fragmented nucleus, pyknosis, loss of membrane integrity, increased empty spaces, and vacuolization in malathion treated granulosa cells. Ethidium bromide/acridine orange (EB/AO) fluorescence staining demonstrated a significant increase in incidence and percentage of apoptosis after malathion exposure (p < 0.001), both between and within the groups. Malathion exposure also resulted in increased DNA fragmentation and decline in both antioxidant enzymes activity namely catalase (CAT) and superoxide dismutase (SOD) in granulosa cells of antral follicles. Moreover, there was found a significant negative correlation between the apoptosis incidence and the level of antioxidant enzymes activity, SOD (r = -0.73 p < 0.01) and CAT (r = -0.80 p < 0.01), in malathion treated ovarian antral follicles. Thus, highlighting the role of DNA fragmentation and declining antioxidant level as a possible mechanism underlying malathion induced reproductive toxicity. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1944-1954, 2016.

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Endocrine-disrupting and cytotoxic potential of anticholinesterase insecticide, diazinon in reproductive toxicity of male mice

Cited by 31 publications

References 53 publications

Synergistic protective role of ceftriaxone and ascorbic acid against subacute diazinon-induced nephrotoxicity in rats

Synergistic protective role of ceftriaxone and ascorbic acid against subacute diazinon-induced nephrotoxicity in rats

Impact of vitamin D deficiency on mouse sperm structure and function

Granulosa cell apoptosis by impairing antioxidant defense system and cellular integrity in caprine antral follicles post malathion exposure

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