Astaxanthin ameliorates heat stress-induced impairment of blastocyst development In Vitro: –astaxanthin colocalization with and action on mitochondria–

Abstract

Purpose The effects of astaxanthin (Ax) on the in vitro development of bovine embryos cultured under heat stress were investigated in combination with the assessment of its cellular accumulation and action on mitochondrial membrane potential (Δ<m). Methods Bovine ≥8-cell embryos were collected on day 3 after in vitro fertilization and exposed to single (day 4) or repeated (day 4 and 5) heat stress (10 h/day at 40.5°C). Ax was added into culture medium under the repeated heat stress and blastocyst development was evaluated. The cellular uptake of Ax in embryos was examined using bright-field and confocal laserscanning microscopy, and high-performance liquid chromatography. The relationship between Ax and mitochondria localization was assessed using MitoTracker dye. The effects of Ax on ΔΨm were investigated using JC-1 dye. Results Blastocyst development in the repeated heat stress treatment decreased significantly (P<0.05) compared with those in single heat stress or normal thermal treatment. The addition of Ax into culture medium did lead to a significant recovery in blastocyst development in the repeated heattreated group. Ax was detected in cytoplasm of embryos and observed to colocalize with mitochondria. Ax recovered ΔΨm in embryos that was decreased by the heat treatment. Conclusions Ax ameliorated the heat stress-induced impairment of blastocyst development. Our results suggest that the direct action of Ax on mitochondrial activity via cellular uptake is a mechanism of the ameliorating effects.

Astaxanthin Inhibits Mitochondrial Permeability Transition Pore Opening in Rat Heart Mitochondria

“…AST can diminish oxidative stress and maintain the integrity of mitochondria, as well as sustain mitochondrial function, protecting their redox balance [47]. In addition, it was shown that AST significantly decreases physiologically-arising oxidative stress and maintains mitochondria in a more reduced state even after stimulation with H 2 O 2 ; it prevents a drop in membrane potential and increases oxygen consumption by mitochondria [48,49]. Park and coauthors showed that AST treatment increased the mitochondrial content, ATP production, and activity of respiratory chain complexes [50].…”

Cellular and epigenetic changes induced by heat stress in bovine preimplantation embryos

“…Development to the blastocyst stage was not compromised in bovine embryos > 8‐cell stage subjected to 40.5°C for 10 hr on Day 4 after insemination. In contrast, exposure to the same heat shock on Days 4 and 5 after insemination reduced blastocyst development from 40.6% in the control group to 21.5% in the heat‐shocked group (Kuroki et al, ). Exposure of 8‐cell embryos to 41°C for 6 hr reduced the proportion of embryos that reached the blastocyst stage (Sakatani, Yamanaka, Kobayashi, & Takahashi, ).…”

Maternal control of oocyte quality in cattle “a review”

“…HS produces excessive ROS, induces apoptosis, and/or reduces the mitochondrial membrane potential in bovine oocytes (Soto and Smith, 2009). In an effort to reduce the oxidative stress in oocytes associated with hyperthermia, using of antioxidants such as folic acid (Koyama et al, 2012), purple sweet potato anthocyanins (Sakatani et al, 2007), Astaxanthin, acarotenoid substance, added to the embryo culture medium (Kuroki et al, 2013), and in vivo administration of antioxidant epigallocatechin gallate significantly improved the blastocyst formation rate and decreased the ROS levels of the heat-shocked embryos. Heat-induced oocyte DNA fragmentation (TUNEL positive) can also be reversed by supplementation of IVM medium with apoptotic cascade inhibitor agents (Roth and Hansen, 2004a), sphingosine 1-phosphate (Roth and Hansen, 2004b), or a BH4 peptide (Soto and Smith, 2009).…”