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International Journal of Medical Laboratory
Shahid Sadoughi University of Medical Sciences
Thu, Oct 30, 2025
[Archive]
Sadaf Saeedi 
, Mohammadamin Ashrafzadeh , Kian Kashani , Seyedeh Zeinab Peighambarzadeh , Maryam Sahebi Ala , Hazhir Khoram , Ali Olfati *
, Mohammadamin Ashrafzadeh , Kian Kashani , Seyedeh Zeinab Peighambarzadeh , Maryam Sahebi Ala , Hazhir Khoram , Ali Olfati *
Clinical Research Development Center, Motazedi Hospital, Kermanshah University of Medical Science, Kermanshah, Iran
Abstract: (113 Views)
Introduction: Arsenic is a potent environmental toxin associated with male infertility. Taurine (TAU) has been demonstrated to regulate oxidative stress biomarkers and improve mitochondrial function.
Materials and Methods: It evaluated the hypothesis that TAU could recover spermatogenesis dysfunction in an arsenic-treated rat model. Then, 24 adult male rats were challenged as follows (n=6/group) for 35 consecutive days: control (distilled water; gavage); 3 mg/l/day sodium arsenite; TAU (1000 mg/kg; 14) during arsenic exposure; and TAU during the study period. 24 h after the last treatment, animals were euthanized, serum samples were processed for assessing sex hormone levels, and testes were processed for weight, oxidative stress indices, histopathology, and RNA extraction for expression levels of autophagic marker genes.
Results: Arsenic causes defective pathologic effects, and upregulates autophagic marker gene expression and production of free radicals. TAU exposure notably ameliorated the autophagy dysregulation through downregulation of the autophagic genes by inhibition of oxidative changes.
Conclusion: This study presents a novel scientific approach to arsenic spermatogenesis dysfunction, attributed to TAU’s antioxidant activity.
Materials and Methods: It evaluated the hypothesis that TAU could recover spermatogenesis dysfunction in an arsenic-treated rat model. Then, 24 adult male rats were challenged as follows (n=6/group) for 35 consecutive days: control (distilled water; gavage); 3 mg/l/day sodium arsenite; TAU (1000 mg/kg; 14) during arsenic exposure; and TAU during the study period. 24 h after the last treatment, animals were euthanized, serum samples were processed for assessing sex hormone levels, and testes were processed for weight, oxidative stress indices, histopathology, and RNA extraction for expression levels of autophagic marker genes.
Results: Arsenic causes defective pathologic effects, and upregulates autophagic marker gene expression and production of free radicals. TAU exposure notably ameliorated the autophagy dysregulation through downregulation of the autophagic genes by inhibition of oxidative changes.
Conclusion: This study presents a novel scientific approach to arsenic spermatogenesis dysfunction, attributed to TAU’s antioxidant activity.
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