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Combined effects of chronic hyperglycaemia and oral aluminium intoxication on testicular tissue and some male reproductive parameters in Wistar rats
Author(s) -
Akinola O. B.,
Biliaminu S. A.,
Adedeji O. G.,
Oluwaseun B. S.,
Olawoyin O. M.,
Adelabu T. A.
Publication year - 2016
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.12512
Subject(s) - streptozotocin , medicine , endocrinology , sperm , diabetes mellitus , testosterone (patch) , spermatogenesis , sperm motility , follicle stimulating hormone , hormone , histology , biology , luteinizing hormone , andrology
Summary Exposure to either environmental toxicants or chronic hyperglycaemia could impair male reproductive function. However, the extent to which exposure to such toxicants, in the presence of pre‐existing metabolic dysfunction, could affect male reproduction is unclear. Streptozotocin‐induced diabetic Wistar rats (12 weeks old) were exposed to oral aluminium chloride at 250 ppm for 30 days; followed by evaluation of caudal epididymal sperm count and motility, assay for serum follicle stimulating hormone (FSH), testosterone (T) and oestradiol; and assessment of testicular histology. Moreover, blood glucose was evaluated by the glucose oxidase method. In rats treated with streptozotocin (STZ) or aluminium (Al) alone, erosion of testicular parenchyma and stroma was observed. This effect was most severe in diabetic rats simultaneously exposed to Al; coupled with reduced caudal epididymal sperm count that was least in this (STZ+Al) group (18.75 × 10 6  ml −1 ) compared with controls (61.25 × 10 6  ml −1 ; P  < 0.05), STZ group or Al group. Moreover, these reproductive perturbations (in the STZ+Al group) were associated with reduced sperm motility and significantly reduced serum FSH ( P  < 0.05); but elevated serum T and oestradiol ( P  < 0.05), compared with control. These suggest that diabetes‐induced testicular lesion is exacerbated by simultaneous oral Al toxicity in Wistar rats.

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