Carvacrol Reduces Mercuric Chloride-Induced Testicular Toxicity by Regulating Oxidative Stress, Inflammation, Apoptosis, Autophagy, and Histopathological Changes.

Hasan Şimşek, Cihan Gür, Sefa Küçükler, Mustafa İleritürk, Nurhan Akaras, Mehmet Öz, Fatih Mehmet Kandemir
Author Information
  1. Hasan Şimşek: Department of Physiology, Faculty of Medicine, Aksaray University, Aksaray, Turkey. hasansimsek@aksaray.edu.tr. ORCID
  2. Cihan Gür: Department of Veterinary Biochemistry, Faculty of Veterinary, Atatürk University, Erzurum, Turkey.
  3. Sefa Küçükler: Department of Veterinary Biochemistry, Faculty of Veterinary, Atatürk University, Erzurum, Turkey.
  4. Mustafa İleritürk: Department of Animal Science, Horasan Vocational College, Ataturk University, Erzurum, Turkey.
  5. Nurhan Akaras: Department of Histology and Embryology, Faculty of Medicine, Aksaray University, Aksaray, Turkey.
  6. Mehmet Öz: Department of Physiology, Faculty of Medicine, Aksaray University, Aksaray, Turkey.
  7. Fatih Mehmet Kandemir: Department of Medical Biochemistry, Faculty of Medicine, Aksaray University, Aksaray, Turkey.

Abstract

Mercuric chloride (HgCl) is a heavy metal that is toxic to the human body. Carvacrol (CAR) is a flavonoid found naturally in plants and has many biological and pharmacological activities including anti-inflammatory, antioxidant, and anticancer activities. This study aimed to investigate the efficacy of CAR in HgCl-induced testicular tissue damage. HgCl was administered intraperitoneally at a dose of 1.23 mg/kg body weight alone or in combination with orally administered CAR (25 mg/kg and 50 mg/kg body weight) for 7 days. Biochemical and histological methods were used to investigate oxidative stress, inflammation, apoptosis, and autophagy pathways in testicular tissue. CAR treatment increased HgCl-induced decreased antioxidant enzyme (SOD, CAT, and GPx) activities and GSH levels. In addition, CAR reduced MDA levels, a marker of lipid peroxidation. CAR decreased the levels of inflammatory mediators NF-κB, TNF-α, IL-1β, COX-2, iNOS, MAPK14, MAPK15, and JNK. The increases in apoptotic Bax and Caspase-3 with HgCl exposure decreased with CAR, while the decreased antiapoptotic Bcl-2 level increased. CAR reduced HgCl-induced autophagy damage by increasing Beclin-1, LC3A, and LC3B levels. Overall, the data from this study suggested that testicular tissue damage associated with HgCl toxicity can be mitigated by CAR administration.

Keywords

References

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MeSH Term

Male
Mercuric Chloride
Oxidative Stress
Cymenes
Autophagy
Apoptosis
Animals
Inflammation
Testis
Rats
Antioxidants
Rats, Wistar

Chemicals

Mercuric Chloride
Cymenes
carvacrol
Antioxidants

Word Cloud

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