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Herein, the point of the study was to examine the defensive impact of NGN on testicular dysfunction initiated by lead. Seventy\u2010Two male Wistar rats were allotted into nine groups; control group, drug control groups, lead acetate group, as well as NGN treated groups (10, 25, and 50\u2009mg\/kg) respectively, given 5 days before lead acetate treatment. The result showed clearly the impact of lead on reduced sperm count, sperm motility as well as serum testosterone and LH levels. Additionally, it caused a significant rise in testicular inflammatory markers TNF\u2010\u03b1, IL\u20101\u03b2, and TGF\u03b2, effects that were accompanied by a reduction of AKT and mTOR levels. Lead acetate also caused degenerative changes in the testis, atrophy, and loss of spermatogenic series. Our findings revealed that NGN in a dose\u2010dependent manner improved spermiotoxicity induced by lead acetate via restoration of the testicular function, preservation of spermatogenesis, halting inflammatory cytokines along with the enhancement of germ cell survival using upregulation of AKT\/mTOR expressions. The present study discloses that NGN suppresses lead acetate toxicity that is involved in the antioxidant effect in a dose\u2010dependent manner,\u00a0besides its anti\u2010inflammatory property.<\/jats:p>","DOI":"10.1002\/jbt.23335","type":"journal-article","created":{"date-parts":[[2023,2,21]],"date-time":"2023-02-21T06:04:09Z","timestamp":1676959449000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Naringenin alleviate reproductive toxicity evoked by lead acetate via attenuation of sperm profile and biochemical alterations in male Wistar rat: Involvement of TGF\u03b2\/AKT\/mTOR pathway"],"prefix":"10.1002","volume":"37","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1835-5806","authenticated-orcid":false,"given":"Alzahraa A.","family":"Elhemiely","sequence":"first","affiliation":[{"name":"The Department of Pharmacology Egyptian Drug Authority, EDA, Formerly NODCAR Giza Egypt"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rania","family":"Yahia","sequence":"additional","affiliation":[{"name":"The Department of Pharmacology Egyptian Drug Authority, EDA, Formerly NODCAR Giza Egypt"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6175-184X","authenticated-orcid":false,"given":"Amany M.","family":"Gad","sequence":"additional","affiliation":[{"name":"The Department of Pharmacology Egyptian Drug Authority, EDA, Formerly NODCAR Giza Egypt"},{"name":"The Department of Pharmacology and Toxicology, Faculty of Pharmacy Sinai University\u2010Kantara Branch Ismailia Egypt"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2023,2,20]]},"reference":[{"key":"e_1_2_11_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuro.2010.09.004"},{"key":"e_1_2_11_3_1","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.10028"},{"key":"e_1_2_11_4_1","doi-asserted-by":"publisher","DOI":"10.1001\/jama.289.12.1523"},{"key":"e_1_2_11_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2019.05.067"},{"key":"e_1_2_11_6_1","doi-asserted-by":"publisher","DOI":"10.1002\/tox.22545"},{"key":"e_1_2_11_7_1","doi-asserted-by":"publisher","DOI":"10.5958\/0974-360X.2018.00228.7"},{"issue":"5","key":"e_1_2_11_8_1","volume":"5","author":"Haouas Z.","year":"2014","journal-title":"J. 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