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Organophosphorus pesticide quinalphos (Ekalux 25 E.C.) reduces sperm functional competence and decreases the fertilisation potential in Swiss albino mice
Author(s) -
Kumari Sandhya,
Dcunha Reyon,
Sanghvi Sahil Piyush,
Nayak Guruprasad,
Kalthur Sneha Guruprasad,
Raut Sushil Yadaorao,
Mutalik Srinivas,
Siddiqui Sazada,
Alrumman Sulaiman A.,
Adiga Satish Kumar,
Kalthur Guruprasad
Publication year - 2021
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/and.14115
Subject(s) - blastocyst , sperm , andrology , quinalphos , fertilisation , sperm motility , reproductive toxicity , organophosphate , oxidative stress , medicine , endocrinology , chemistry , biology , toxicity , pesticide , embryogenesis , biochemistry , reproductive technology , agronomy , gene
Quinalphos (QP) is one of the most commonly used organophosphate pesticide for agriculture. In this study, adult Swiss albino male mice were orally administered with 0.25, 0.5 and 1.0 mg/kg of QP (Ekalux 25 E.C.) for ten consecutive days and the reproductive function was assessed at 35 and 70 days after QP treatment. At highest dose (1.0 mg/kg), QP exposure resulted in significant decrease in motility and increase in sperm head defects and DNA damage. Pharmacokinetic data showed a threefold increase in concentration of QP in the testis as compared to serum. QP was detectable in testes even after 24 hr of administration indicating slow clearance from tissue. In addition, high oestradiol, low testosterone level with a parallel increase in aromatase and cytochrome P450 transcript levels was observed. Significant decrease in fertilisation, lower blastocyst rate and poor blastocyst quality was observed when spermatozoa collected from QP exposed mice were subjected to in vitro fertilisation. In conclusion, exposure of QP to male mice decreases the sperm functional competence and fertilising ability, which appears to be mediated through elevated oxidative stress and altered steroidogenesis in testes.

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