Turmeric and vitamin C mitigate testicular atrophy induced by lead diacetate via regulation of GRP-78/17β-HSD pathways in rat's model.
Laila Mohamed FaddaReem AlsharidahIman Huseein HasanPublished in: Andrologia (2021)
Occupational and ecological contacts to lead persist as a universal concern. Lead alters most of the physiological processes via enhancing oxidative stress. Thus, this study was purposed to assess the influence of turmeric (TMRC) and/or vitamin C (VIT-C) on Lead diacetate (Lead diAC)-induced testicular atrophy with an emphasis on oxidative stress, inflammation, BAX/STAR and GRP-78/17β-HSD signalling. Rats were injected with Lead diAC and then treated with TMRC and/or VIT-C orally for 1 week. Lead diAC decreased serum testosterone and testicular glutathione levels. It also decreased superoxide dismutase activity. On the contrary, levels of malondialdehyde, tumour necrosis factor-α, IL-1β and caspase-3 were increased. mRNA levels and protein expressions of GRP-78 and BAX were upregulated, while the expression of both steroidogenic acute regulatory protein and 17β-HSD were downregulated. DNA fragmentation was increased as well. These changes were further confirmed by histopathological findings. Supplementation with TMRC and/or VIT-C ameliorated all of the above parameters. In Conclusion: TMRC or VIT-C specially in combination group prevents Lead diAC testicular damage via reduction of oxidative injury as well as inflammation, downregulation of GRP-78/BAX and upregulation of 17β-HSD and STAR expression as well as improvement in the histological architecture of the testis.
Keyphrases
- oxidative stress
- induced apoptosis
- endoplasmic reticulum stress
- poor prognosis
- diabetic rats
- germ cell
- binding protein
- dna damage
- signaling pathway
- transcription factor
- randomized controlled trial
- liver failure
- cell surface
- cell death
- ischemia reperfusion injury
- hepatitis b virus
- intensive care unit
- long non coding rna
- drug induced
- risk assessment
- nitric oxide
- circulating tumor
- small molecule
- acute respiratory distress syndrome
- study protocol
- double blind
- circulating tumor cells
- amino acid