ArticleMolecular biology reports2021
The protective role of Coenzyme Q10 in metallothionein-3 expression in liver and kidney upon rats' exposure to lead acetate.
Article in Molecular biology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Coenzyme Q10 and Xenobiotic Metabolism: An Overview.International journal of molecular sciences · 2025Review
- Lead exposure promotes NF2-wildtype meningioma cell proliferation through the Merlin-Hippo signaling pathway.Environmental health and preventive medicine · 2025Article
- Protective Role of Myricetin and Fisetin Against Nephrotoxicity Caused by Lead Acetate Exposure through Up-regulation of Nrf2/HO-1 Signalling Pathway.Biological trace element research · 2024Article
- Heavy Metal Exposure: Molecular Pathways, Clinical Implications, and Protective Strategies.Antioxidants (Basel, Switzerland) · 2024Review
- Evaluation of the potential of miR-21 as a diagnostic marker for oocyte maturity and embryo quality in women undergoing ICSI.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metallothionein-3 (MT3) is an antioxidant protein that alters after exposure to heavy metals. In this study, we investigated the hepatic and renal expression of MT3 gene following exposure to lead acetate (PbAc) alone and PbAc plus CoQ10 as an adjuvant antioxidant. Twenty-four rats were allocated into three groups, including control, PbAc (free access to drinking water contaminated with PbAc at 1 g/100 ml), and PbAc plus CoQ10 (10 mg/kg/day Oral). After 28 consecutive days of treatment, the mRNA expression of MT3 and Cyt-c genes and MT3 protein levels were assessed using real-time PCR and immunosorbent assay. The serum lipid profile was also monitored in the three groups. PbAc exposure significantly reduced the hepatic and renal MT3 mRNA and protein expression compared to the control group. This reduction was significantly increased with addition of CoQ10 to levels near those of the control group. The hepatic and renal expression of Cyt-c mRNA increased after treatment with PbAc, while such effect was reversed after addition of CoQ10. Alteration in lipid profile including increased cholesterol and low-density lipoprotein levels were observed after PbAc exposure which were counteracted by CoQ10. Our results confirm the cytotoxic effects of acute lead exposure manifested as changes in the serum lipid profile and cellular levels of Cyt-c mRNA. These cytotoxic effects may have been caused by decreased MT3 gene expression and be reduced by the protective role of CoQ10.
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