Surface-enhanced Raman scattering (SERS), owing to its high sensitivity and rapid response, has been widely used in various fields. However, it is still a challenge to prepare SERS substrates with high stability and reproducibility. Metal–organic frameworks (MOFs), with excellent enrichment capacity and stability, provide a new material for high-performance SERS substrates. In this paper, we prepare a MIL-101­(Cr) film via a secondary growth method, and Ag+ is reduced to Ag NPs by UV irradiation and attach to the film to synthesize the Ag@MIL-101­(Cr) film SERS substrate. Then, we change the time of UV light illumination and the amount of silver nitrate in order to obtain the optimal substrate. The detection capability of this sample can be up to 10–11 M for 4-ATP, and the relative standard deviation (RSD) is only about 5%, which demonstrates that the substrate has excellent SERS effect and reproducibility. Finally, the prepared substrate has been applied for the determination of nitrofurantoin, with its detection capability up to 10–7 M. This work proposes a simple method to synthesize MOF-based film substrate with high SERS performance and uniformity and provides potential for the sensitive detection of chemical or antibiotic residue.

Hepatocellular carcinoma (HCC) is one of the most common types of primary liver cancer and the third most frequent cause of cancer death worldwide. Diethylnitrosamine (DEN) is one of the recognized risk factors for hepatocarcinogenesis likely due to CYP2E1-mediated metabolic activation. However, CYP2E1-mediated DEN metabolic activity in non-neoplastic liver tissue from HCC patients has not been determined; the role of CYP2E1 activity, in particular CYP2E1 constitutive activity and CYP2E1 inhibited activity, with respect to the hepatocarcinogenesis induced by DEN is not yet clear. Herein, we determined CYP2E1-mediated DEN metabolic activity in non-neoplastic liver tissue from HCC patients and found that CYP2E1-mediated DEN metabolic activity was significantly elevated with a 43.3% positive rate, and clinicopathologic parameters did not affect the activity. Then, using a Sprague-Dawley rat liver tumor model induced by DEN, the relationship between CYP2E1 constitutive/inhibited activity and hepatocarcinogenesis was explored. The results showed that the CYP2E1 constitutive activity was strongly correlated with tumor incidence and severity of liver tumorigenesis (nodule numbers and size), whereas inhibition of CYP2E1 activity decreased hepatocyte proliferation, liver injury, and liver carcinogenesis in the presence of DEN. In conclusion, the higher CYP2E1 activity would lead to an increased incidence of HCC as a result of CYP2E1-mediated DEN activation. Therefore, higher CYP2E1 activity might be a risk factor for HCC induced by DEN.

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