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The present study was carried for the toxicological assessment of Cinnamomum tamala essential oil (CTEO) in vivo since no previous work has reported the sub‐chronic toxicity in rats. Hence, the aim of the present study was to study for the first time sub‐chronic toxicity of CTEO, extracted from C. tamala leaves, in Wistar rats. Recently, there is development of new food preservatives to increase the shelf life of food. The incorporation of CTEO as a food preservative could be a good alternative to synthetic compounds. For decades, C. tamala and its leaves are being used in food and pharmaceutical preparation. In order to fulfill the requirements suggested by the Scientific Committee on Food for safety assessment of substances used in food contact materials, sub‐chronic studies are needed. Therefore, in vivo experiments have been conducted to assess the antidiabetic and antioxidant properties of CTEO, which also demands toxicity assessment. Practical applications Medicinal plants and herbs have been used since ancient times for their formulations and essential oils (EOs). Several studies have investigated the composition of EOs and plant extracts having nutritional and medicinal properties. Cinnamomum tamala essential oil (CTEO) is used in the food and pharmaceutical preparations as well as in traditional medicinal systems as a preservative and curative agent in various alignments. In the present study, the oral acute and sub‐chronic toxicity of CTEO was assessed in Wistar rats, including the clinical, hematological, biochemical and pathological parameters. The repeated oral administration of CTEO showed no mortality, alterations in food and water intake, body weight, hematology and biochemistry, organ weight and histopathology. In conclusion, the use of CTEO in food and other pharmaceutical preparations may be safe due to its lack of toxicity in Wistar rats during the period of study.

Background: Cancer is caused by three factors: Nutrition, inflammation and cigarette smoke. This study in rat experimental models would enable us to understand the mechanism of lung cancer caused by NNK to which humans are continuously exposed, help us understand possible molecular targets, design drugs for humans against lung cancer. Aim: A lung cancer model was developed by administering tobacco specific carcinogen: NNK [4-methylnitrosamino)-1-(3-pyridyl)-1-butanone] to male wistar rats in 24 weeks. Further, In silico approach was followed to screen the molecular targets. Methods: A method was established in which subcutaneous and intraperitoneal injections of NNK were administered to male wistar rats simultaneously. For authentication of lung cancer in vivo we performed molecular docking simulations with protein biomarkers:Cox-2, p53, p38 MAPKs and EGFR using Hex-Discovery Studio, Schrödinger-maestro software. Results: Lung morphology and histopathology indicated the initiation of bronchiolar epithelial hyperplasia, squamous dysplasia beginning in cancer 1 group after 16 weeks NNK exposure. 66.66% incidence of squamous cell carcinoma (SCC), 33.3% incidence of adenocarcinoma in cancer 2 group after being exposed to NNK. Results indicated that the SCC and adenocarcinoma gradually increased from 66.66% to 85.71% in cancer 2 group and 33.33% to 42.58% in cancer 3 groups respectively. Docking results indicate the total binding energy and glide energy of Cox-2, p53, p38 MAPKs, EGFR : 38.14, -211.58, -181.58, - 213.05 Kcal/mol and -39.25, -32.16,-36.49, -40.19 Kcal/mol, respectively. Conclusion: Pulmonary adenocarcinoma developed in 24 weeks, in silico experiments confirm EGFR to be the most potential target for NNK induced lung Cancer.

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