Abstract

In vitro toxicity of carbon dots (CDs) in unfried and fried breadcrumbs was evaluated using NRK cells to analyze the harm of excessive frying and the factors causing the increase of toxicity during processing and cooking. The results showed that the toxicity of CDs in market breadcrumbs increased by an astonishing 230 times after frying at 180 °C. Subsequent experiments showed that cell cycle was arrested at the G0/G1 phase when NRK cells were treated with CDs, which ultimately led to apoptosis and necrosis. The mechanism was identified as CDs-induced the production of ROS, resulting in the loss of mitochondrial membrane potential (67.00 ± 1.80%) and triggered early apoptosis. Furthermore, the release of inclusions from necrotic cell lysis led to the synthesis of upstream mediators HMGB-1 and TGF-β1, which increased downstream pro-inflammatory factors (TNF-α, IL-1β, and IL-6) and decreased anti-inflammatory factor (IL-10). The main measure to reduce toxicity was to control the amount of sucrose added. These results were useful in understanding the negative impact of excessively fried food and provided an idea for reducing the production of food-borne CDs.

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