Modulation of redox homeostasis by Lamiaceae herbs in seminal vesicles of Lumbricus terrestris

Abstract

a b s t r a c tBackground/Aims: Health benefits of Lamiaceae herbs are attributed to the presence of antioxidant phytochemicals. However, mechanism of in vivo functionality is not very well understood. We determined the in vivo effect of dietary Lamiaceae herbs on modulating redox-nitric oxide (NO) homeostasis and sperm quality in oxidation prone environment of seminal vesicles in Lumbricus terrestris. Methods: Animals fed ad libitum on Lumbricus growth medium supplemented with 0% (control), 0.1% or 0.5% (w/v) of different herbs. The seminal vesicles of the animal were dissected out on day 2 and day 6, and gently disrupted. Levels of malondialdehyde (MDA), DNA fragmentation (DNAF), glutathione (GSH), nitrates/nitrites (NOx), superoxide dismutase (SOD), catalase (CAT) were determined using standard assays. Sperm maturity and deformation (DFO) was quantified microscopically. Results: Overall, the herb treatments decreased MDA levels by (60e90%), increased SOD activity (15e50%), and decreased DNAF (6e11%). Treatments with basil and oregano at 0.1% (w/v) were most effective. Conclusion: Our suggests that phytochemicals from Lamiaceae herbs modulate redox stress response, and protect against oxidative stress in seminal vesicles.

Ginnalin A Binds to the Subpockets of Keap1 Kelch Domain To Activate the Nrf2-Regulated Antioxidant Defense System in SH-SY5Y Cells

“…Exogenous antioxidants can protect neurons from oxidative stress. , In a large community study published in 2020, dietary intake of flavonoids, a class of natural polyphenols known to possess antioxidant and anti-inflammatory properties, appears to reduce the risk of AD dementia . These antioxidative agents either react directly with ROS before they wreak havoc to neurons or induce upregulated expression of endogenous antioxidants to maintain redox homeostasis in the cellular milieu. − Regarding the latter, neurons have developed different defense mechanisms, one of which is the nuclear factor erythroid-2 related factor 2 (Nrf2)/antioxidant response element (ARE) pathway to counteract detrimental effects of ROS. , In the quiescent cellular state, Nrf2 binds strongly to the Kelch-like ECH-associated protein 1 (Keap1) homodimer, which facilitates the ubiquitin-dependent proteasomal degradation of Nrf2 through a Cullin-based E3 (CUL-E3) ligase complex . In cells under oxidative stress, the Keap1–Nrf2 interaction is weakened and Nrf2 disassociates from Keap1 to abort proteasomal degradation.…”