Hesperidin Protects Alcohol-induced Mitochondrial Abnormalities via the Inhibition of Oxidative Stress and MPT Pore opening in Newborn Male Rats as Fetal Alcohol Syndrome Model
OBJECTIVE: Prenatal alcohol exposure causes fetal developmental abnormalities via mitochondrial dysfunction, ROS formation, oxidative stress. Therefore, we aimed to investigate the potential of hesperidin as a mitochondrial protective and anti-oxidative agent in newborn male rats as fetal alcohol syndrome (FAS) model.
METHODS: Newborns male rats were divided randomly into 5 groups; sham group (receiving 27.8 ml/kg milk solution, orally), ethanol group (5.25 g/kg, orally, 2-10 days after birth in milk solution), ethanol + hesperidin group (25 mg/kg per day orally), ethanol + hesperidin group (50 mg/kg per day orally), and ethanol + hesperidin group (100 mg/kg per day orally). Thirty-six days after birth, newborns male rats were sacrificed and brain mitochondria were isolated using differential centrifugation. Mitochondrial toxicity biomarkers of including: succinate dehydrogenases (SDH) activity, mitochondrial swelling, mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) were measured.
RESULTS: Offspring neonatally exposed to ethanol showed a significant reduction of SDH activity, mitochondrial swelling, MMP collapse, induction of ROS formation and lipid peroxidation in isolated mitochondria. Orally administration of hesperidin restored SDH activity, improved MMP collapse, mitochondrial swelling, and reduced ROS formation.
CONCLUSIONS: This study demonstrates that hesperidin exerts a potent mitochondria protective effect against alcohol-induced mitochondrial toxicity in FAS model. Moreover, these findings indicates that hesperidin might be a useful compound for prevention of alcohol-induced fetal developmental abnormalities during pregnancy.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2023 |
|---|---|
| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - year:2023 |
|---|---|
| Enthalten in: |
Journal of studies on alcohol and drugs - (2023) vom: 26. Dez. |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Jamali, Zhaleh [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Brain |
|---|
| Anmerkungen: |
Date Revised 26.12.2023 published: Print-Electronic Citation Status Publisher |
|---|
| doi: |
10.15288/jsad.23-00243 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM366377507 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM366377507 | ||
| 003 | DE-627 | ||
| 005 | 20231227141351.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231227s2023 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.15288/jsad.23-00243 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1239.xml |
| 035 | |a (DE-627)NLM366377507 | ||
| 035 | |a (NLM)38147083 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Jamali, Zhaleh |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Hesperidin Protects Alcohol-induced Mitochondrial Abnormalities via the Inhibition of Oxidative Stress and MPT Pore opening in Newborn Male Rats as Fetal Alcohol Syndrome Model |
| 264 | 1 | |c 2023 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Revised 26.12.2023 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status Publisher | ||
| 520 | |a OBJECTIVE: Prenatal alcohol exposure causes fetal developmental abnormalities via mitochondrial dysfunction, ROS formation, oxidative stress. Therefore, we aimed to investigate the potential of hesperidin as a mitochondrial protective and anti-oxidative agent in newborn male rats as fetal alcohol syndrome (FAS) model | ||
| 520 | |a METHODS: Newborns male rats were divided randomly into 5 groups; sham group (receiving 27.8 ml/kg milk solution, orally), ethanol group (5.25 g/kg, orally, 2-10 days after birth in milk solution), ethanol + hesperidin group (25 mg/kg per day orally), ethanol + hesperidin group (50 mg/kg per day orally), and ethanol + hesperidin group (100 mg/kg per day orally). Thirty-six days after birth, newborns male rats were sacrificed and brain mitochondria were isolated using differential centrifugation. Mitochondrial toxicity biomarkers of including: succinate dehydrogenases (SDH) activity, mitochondrial swelling, mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) were measured | ||
| 520 | |a RESULTS: Offspring neonatally exposed to ethanol showed a significant reduction of SDH activity, mitochondrial swelling, MMP collapse, induction of ROS formation and lipid peroxidation in isolated mitochondria. Orally administration of hesperidin restored SDH activity, improved MMP collapse, mitochondrial swelling, and reduced ROS formation | ||
| 520 | |a CONCLUSIONS: This study demonstrates that hesperidin exerts a potent mitochondria protective effect against alcohol-induced mitochondrial toxicity in FAS model. Moreover, these findings indicates that hesperidin might be a useful compound for prevention of alcohol-induced fetal developmental abnormalities during pregnancy | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Brain | |
| 650 | 4 | |a Developmental Toxicity | |
| 650 | 4 | |a Flavanone | |
| 650 | 4 | |a Natural Products | |
| 650 | 4 | |a Teratogenic Effects | |
| 700 | 1 | |a Salimi, Ahmad |e verfasserin |4 aut | |
| 700 | 1 | |a Garmabi, Behzad |e verfasserin |4 aut | |
| 700 | 1 | |a Khezri, Saleh |e verfasserin |4 aut | |
| 700 | 1 | |a Khaksari, Mehdi |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Journal of studies on alcohol and drugs |d 2007 |g (2023) vom: 26. Dez. |w (DE-627)NLM167005537 |x 1938-4114 |7 nnns |
| 773 | 1 | 8 | |g year:2023 |g day:26 |g month:12 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.15288/jsad.23-00243 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |j 2023 |b 26 |c 12 | ||