Abstract
1,3-Dichloro-2-propanol (1,3-DCP) is a food processing contaminant and has been shown to perturb male reproductive function. Cyanidin-3-O-glucoside (C3G), an anthocyanin antioxidant, is reported to have protective effects on many organs. However, it remains unclear whether C3G protects against chemical-induced reproductive toxicity. The present study was therefore to investigate the intervention of C3G on 1,3-DCP-induced reproductive toxicity in R2C Leydig cells. Results demonstrated that C3G inhibited the 1,3-DCP-induced cytotoxicity and cell shape damage with the effective doses being ranging from 10 to 40 μmol/L. In addition, 1,3-DCP (2 mmol/L) exposure significantly increased the ROS level and mitochondrial membrane potential damage ratio, leading to a decrease in progesterone production, while C3G intervention reduced the ROS level, and increased the progesterone production after 24 h treatment. Most importantly, C3G intervention could up-regulate the cyclic adenosine monophosphate (cAMP) level and protein expression of steroidogenic acute regulatory protein and 3β-hydroxysteroid dehydrogenase. It was concluded that C3G is effective in reducing 1,3-DCP-induced reproductive toxicity via activating steroidogenic enzymes and cAMP level.
Highlights
In recent years, food chemical contaminants have attracted more and more attention. 1,3-Dichloro2-propanol (1,3-DCP) is one of them
The cell viability decreased with the increase of 1,3-DCP concentration of 0, 1, 2, 4, 6, and 8 mmol/L (Figure 2A) At the dosage of 2 mmol/L, the cell viability decreased to 48.7%
The results showed that C3G intervention, especially at the concentration of 20 and 40 μM, significantly reversed 1,3-DCP -induced cytotoxicity in R2C cells (Figure 2D)
Summary
Food chemical contaminants have attracted more and more attention. 1,3-Dichloro2-propanol (1,3-DCP) is one of them. It is produced in the processing, cooking, and storage of many foodstuffs such as soy sauce, oyster sauce, acid-hydrolyzed vegetable proteins, and processed meat products due to reaction of chloride ions with lipid components in foods (Velisek et al, 1978; Kim et al, 2015). The Joint FAO/WHO Expert Committee on Food Additives (JECFA) has concluded that 1,3DCP is a genotoxic carcinogen, and leads to tumor development in various organs. Epidemiological data are still unavailable, anda tolerable daily intake for 1,3-DCP has not been established (The Joint FAO-WHO Expert Committee Report on Food Additives [JECFA], 2001). According to the JECFA assessment, mean and 95th percentile dietary exposure estimates for 1,3-DCP in various foods were 0.008–0.051 μg/kg bw/day and 0.025–0.136 μg/kg bw/day, respectively, in population (The Joint FAO-WHO Expert Committee Report on Food Additives [JEFCA], 2007). 1,3-DCP was found to reduce the progesterone production by inhibiting the activity of steroidogenic enzymes and decreasing cAMP level in Rat Leydig cells (R2C) (Sun et al, 2014)
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