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Effect of quercetin on cadmium chloride-induced impairments in sexual behaviour and steroidogenesis in male Wistar rats

Ujah GA, Nna VU, Agah MI, Omue LO, Leku CB, Osim EE

Andrologia, 2018 Mar;50(2).
PMID: 28703286 DOI: 10.1111/and.12866

Cadmium chloride (CdCl2 ) has been reported to cause reproductive toxicity in male rats, mainly through oxidative stress. This study examined its effect on sexual behaviour, as one of the mechanisms of reproductive dysfunction, as well as the possible ameliorative effect of quercetin (QE) on same. Thirty male Wistar rats (10 weeks old), weighing 270-300 g, were used for this study. They were either orally administered 2% DMSO, CdCl2 (5 mg/kg b.w.), QE (20 mg/kg b.w.) or CdCl2 +QE, once daily for 4 weeks, before sexual behavioural studies. The 5th group received CdCl2 for 4 weeks and allowed 4-week recovery period, before sexual behavioural test. Rats were sacrificed after sexual behavioural studies. The blood, testis and penis were collected for biochemical assays. Cadmium increased mount, intromission and ejaculatory latencies, but reduced their frequencies, compared to control. Serum nitric oxide increased, while penile cyclic guanosine monophosphate reduced in the CdCl2 -exposed rats, compared to control. CdCl2 increased testicular cholesterol, but reduced 3β-hydroxysteroid dehydrogenase (3β-HSD) and 17β-HSD activities, and testosterone concentration. QE better attenuated these negative changes compared to withdrawal of CdCl2 treatment. In conclusion, CdCl2 suppressed steroidogenesis, penile erection and sexual behaviour, with poor reversal following withdrawal, while QE attenuated these effects.
Cadmium chloride-induced testicular toxicity in male wistar rats; prophylactic effect of quercetin, and assessment of testicular recovery following cadmium chloride withdrawal

Nna VU, Ujah GA, Mohamed M, Etim KB, Igba BO, Augustine ER, et al.

Biomed Pharmacother, 2017 Oct;94:109-123.
PMID: 28756368 DOI: 10.1016/j.biopha.2017.07.087

This study assessed the effect of quercetin (QE) on cadmium chloride (CdCl2) - induced testicular toxicity, as well as the effect of withdrawal of CdCl2 treatment on same. Thirty male Wistar rats aged 10 weeks old and weighing 270-300g were assigned into 5 groups and used for this study. Rats in groups 1-4 were administered vehicle, CdCl2 (5mg/kg bwt), CdCl2+QE (5mg/kg bwt and 20mg/kg bwt, respectively) or QE (20mg/kg bwt) orally for 4 weeks. Group 5 rats received CdCl2, with 4 weeks recovery period. Results showed that cadmium accumulated in serum, testis and epididymis, decreased body weight, testicular and epididymal weights, sperm count, motility and viability. Cadmium decreased serum concentrations of reproductive hormones, but increased testicular glucose, lactate and lactate dehydrogenase activity. Cadmium decreased testicular enzymatic (superoxide dismutase, catalase and glutathione peroxidase) and non-enzymatic (glutathione, vitamins C and E) antioxidants, and increased malondialdehyde and hydrogen peroxide. Cadmium down-regulated Bcl-2 protein, up-regulated Bax protein, increased Bax/Bcl-2 ratio and cleaved caspase-3 activity. Histopathology of the testis showed decreased Johnsen's score and Leydig cell count. These negative effects were attenuated by QE administration, while withdrawal of CdCl2 did not appreciably reverse toxicity. We conclude that QE better protected the testis from CdCl2 toxicity than withdrawal of CdCl2 administration.
Maternal Geophagy of Calabash Chalk on Foetal Cerebral Cortex Histomorphology

Ekanem TB, Ekong MB, Eluwa MA, Igiri AO, Osim EE

Malays J Med Sci, 2015 12 31;22(4):17-22.
PMID: 26715904

BACKGROUND: Calabash chalk, a kaolin-base substance is a common geophagic material mostly consumed by pregnant women. This study investigated its effect on the histomorphology of the foetal cerebral cortex.
METHODS: Twelve gestating Wistar rats were divided equally into groups 1 and 2. On pregnancy day seven (PD7), group 2 animals were administered 200 mg/kg body weight of calabash chalk suspension, while group 1 animals served as the control and received 1 ml of distilled water, by oral gavages and for 14 days (PD7-PD20). On PD21, the dams were sacrificed, and the foetuses removed, examined for gross malformations, weighed and culled to two foetuses per mother. Their whole brains were excised, weighed and preserved using 10% buffered formalin, and routinely processed by haematoxylin and eosin, and Luxol fast blue methods.
RESULTS: The foetuses showed no morphological change, but their mean body weights was higher (p=0.0001). Histomorphological sections of the cerebral cortex showed hypertrophy and hyperplasia of cells in all the cortical layers, with less demonstrated Nissl and higher (p=0.001) cellular population compared with the control group.
CONCLUSION: Calabash chalk cause body weight increase and histomorphological changes in the cerebral cortex of foetuses.
Tert-butylhydroquinone preserve testicular steroidogenesis and spermatogenesis in cisplatin-intoxicated rats by targeting oxidative stress, inflammation and apoptosis

Nna VU, Ujah GA, Suleiman JB, Mohamed M, Nwokocha C, Akpan TJ, et al.

Toxicology, 2020 08;441:152528.
PMID: 32565124 DOI: 10.1016/j.tox.2020.152528

Cisplatin (Cis) is an effective chemotherapeutic intervention against many cancer types. However, the oxidative stress-related toxicities associated with cancer cell resistance-induced dose scaling has limited its long-term use. In the present study, we explored the benefits of the antioxidant, tert-butylhydroquinone (tBHQ; 50 mg/kg b.w./day, for 14 days) against Cis single dose injection (7 mg/kg b.w., i.p on Day 8), on testicular toxicity of male Wistar rats. Cis triggered testicular and epididymal oxidative stress, testicular inflammation (upregulated NF-κB, TNF-α and IL-1β mRNA levels, and downregulated IL-10 mRNA level), increased testicular apoptosis (increased Bax/Bcl2 and caspase-3 mRNA levels) and decreased testicular germ cells proliferation. Further, Cis decreased testicular steroidogenesis (decreased expression of StAR, CYP11A1, 3β-HSD and 17β-HSD mRNA and proteins) and decreased follicle stimulating hormone, luteinizing hormone and testosterone levels. Cis also decreased sperm count, motility, viability, normal morphology and Johnsen score. However, intervention with tBHQ significantly decreased oxidative stress by upregulating Nrf2 gene, suppressed inflammation, apoptosis and increased testicular germ cells proliferation. tBHQ also increased steroidogenesis and improved sperm parameters. Taken together, tBHQ improves steroidogenesis and spermatogenesis in Cis-intoxicated rats by improving antioxidant status, dampening inflammation and apoptosis, thus improving the proliferative capacity of spermatogenic cells.