article · Andrologia
This study examined the protective effects of royal jelly against testicular toxicity caused by cadmium exposure in male rats. Cadmium chloride administration led to significant reductions in serum testosterone, luteinising hormone, follicle-stimulating hormone, antioxidant enzyme activity, and both sperm count and motility. It also increased oxidative stress markers, inflammatory factors such as tumour necrosis factor-alpha, and sperm abnormalities, alongside causing severe structural damage to the seminiferous tubules. Furthermore, cadmium exposure suppressed the expression of essential steroidogenic enzymes, hormone receptors, and androgen binding protein. Administering royal jelly, either as a pre-treatment or concurrent treatment, greatly reduced these harmful physiological, biochemical, and structural alterations. The findings demonstrate that royal jelly counteracts cadmium-induced testicular dysfunction and oxidative damage in an animal model.
Cadmium is an environmental pollutant capable of damaging male reproductive health and fertility through oxidative stress and hormone disruption. Demonstrating that a natural substance like royal jelly can mitigate these harmful effects highlights potential therapeutic strategies to protect reproductive function against heavy metal toxicity.
This work points to the potential use of royal jelly as a protective therapeutic or nutraceutical agent against heavy metal-induced male infertility. Potential users would include pharmaceutical or dietary supplement developers focusing on reproductive health and toxic exposure mitigation. However, this is early-stage animal research, meaning substantial further clinical testing is required before practical human application.
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This study aimed to investigate the protective potential of Royal jelly (RJ) against cadmium (Cd)-induced testicular dysfunction in rats. Thirty-five adult male Wistar rats were assigned into five groups. G I; (control) injected intraperitoneally with saline, G II injected intraperitoneally with a single dose of CdCl<sub>2</sub> (1 mg/kg BW), G III received RJ (100 mg/kg BW/day) orally, G IV was pre-treated with RJ for 1 week then, treated with CdCl<sub>2</sub> , and G V was co-treated with RJ and CdCl<sub>2</sub> . After day 56, serum and tissue samples were collected and analysed. The results showed decreased serum testosterone, luteinising hormone (LH), follicle-stimulating hormone (FSH), superoxide dismutase, glutathione reductase, sperm motility and count while increased malondialdehyde, nitric oxide, tumour necrosis factor-α (TNF-α) and sperm abnormalities, along with a severely damaged seminiferous tubules epithelium with cytoplasmic and nuclear disruptions following Cd toxicity. Additionally, Cd stimulated testicular mRNA expression of TNF-α while inhibited those of steroidogenic acute regulatory protein, cytochrome P450 cholesterol side chain cleavage enzyme androgen binding protein, FSH-receptor, LH-receptor, androgen receptor, 3β-hydroxysteroid dehydrogenase (HSD), 17β-HSD, and cytochrome P450 17A1. These negative alterations of cadmium were greatly reduced by RJ treatment. This study concluded that RJ protects against Cd-induced testicular toxicity.
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DOI: 10.1111/and.12996
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