4.5 Article

Zinc loaded whey protein nanoparticles mitigate the oxidative stress and modulate antioxidative gene expression in testicular tissues in rats

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ELSEVIER
DOI: 10.1016/j.jddst.2021.102322

Keywords

Whey protein nanoparticles; Zinc citrate; Testicular injury; Oxidative stress; Drug delivery; Gene expression

Funding

  1. National Organization for Drug Control and Research, Giza, Egypt
  2. National Research Centre, Dokki, Cairo, Egypt [12050305]
  3. Konsortium Institut Halal Malaysia (KIHIM) [MOHE18-002-0002]

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The study showed that zinc-loaded WPNPs can effectively protect against CCl4-induced testicular damage, and reduce oxidative stress by regulating the Nrf2-Keap1 antioxidative signaling pathway.
This study aimed to utilize whey protein nanoparticles (WPNPs) and zinc (Zn) loaded WPNPs to protect against carbon tetrachloride (CCl4)-induced testicular damage in rats. Zn was loaded on WPNPs at three levels and Zn release was determined at different time intervals. Seventy male Wistar rats were divided into 7 groups and treated orally for 4 weeks as follows: the control group, CCl4-treated group (0.5 ml/100 g b.w) twice a week, CCl4 plus WPNPs-treated group (300 mg/kg b.w), CCl4 plus Zn citrate-treated group (50 mg/kg b.w), and the groups treated with CCl4 plus the three Zn-WPNPs formulations. Blood and testicular tissue samples were collected for different assays. Animals treated with CCl4 showed a significant decrease in body weight and relative weight of the testis, testosterone level, antioxidant enzymes activity and mRNA expression of Nrf2, HO-1 and NQO1 and increased Malondialdehyde (MDA), nitric oxide (NO) and mRNA expression of Keep1 and induced histological changes in the testis. WPNPs alone, Zn alone or Zn loaded WPNPs at the three levels protect against CCl4-induced testicular damage. These effects were more pronounced in the group received the fabrication with low Zn level. This study concluded that Zn-WPNPs could reduce the oxidative stress in the testicular tissue via different mechanisms mainly via the regulation of Nrf2-Keap1 antioxidative signaling pathway.

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