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The pyrethroid imiprothrin is widely used worldwide for control of insects in the agriculture and public health sectors. No sufficient information is however available concerning detoxification gene expression, i.e., cytochrome P450 1A2 (CYP1A2) and metallothionein 1a gene, oxidative stress, lipid peroxidation, DNA damage, cytotoxicity, genotoxicity, and organ injury induced by imiprothrin in mammals. This study is designed to explain the mechanism of imiprothrin induced detoxification gene expression, DNA damage, cytotoxicity, genotoxicity, and organ toxicity in male rats. The benchmark dose (BMD) was calculated to find the best sensitive markers to imiprothrin toxicity. Imiprothrin was injected intraperitoneally (i.p.) into male rats once a day for 5 days with doses of 19, 38, and 75 mg/kg body weight (b.wt.). Imiprothrin caused a significant increase in lipid peroxidation and changes in oxidative stress biomarkers in treated rats. Significant dose-dependent changes in the liver and kidney biomarkers were observed. Histopathological alterations were seen in the liver and kidney tissue of male rats. Imiprothrin also significantly increased chromosomal aberrations (CA) and micronuclei in bone-marrow cells, and induced lipid peroxidation, oxidative stress, cytotoxicity, and liver and kidney dysfunction, and damage. Imiprothrin induced DNA damage and over detoxification gene expression of CYP1A2 and metallothionein 1a gene in hepatocytes of male rats. Imiprothrin thus shows clastogenic and genotoxic potential. The mechanism for hepatorenal toxicity and injury, genotoxicity/cytotoxicity of imiprothrin might be due to enhanced lipid peroxidation, and oxidative stress associated with overproduction of free radicals, especially reactive oxygen species, and an imbalance in redox status. From the BMD models, aspartate aminotransferase (AST), total protein, uric acid, superoxide dismutase (SOD), and micronuclei (MPEs) were very sensitive markers to imiprothrin toxicity.

Our study investigated the ameliorative effects of thymoquinone (TQ) on the pulmonary blood vessels which were injured after intratracheal administration of Escherichia coli-derived lipopolysaccharide (LPS) in a rat model. Forty rats (150 ± 50 g) were randomly divided into four groups equally. The first group was intratracheally administered LPS (Escherichia coli O55:B5) at a dose 200 μg. The second group was co-administered intraperitoneal injection of TQ and LPS daily for one week. The third group was provided intraperitoneal injection of 1 mg of TQ. The fourth group was administered normal saline intratracheally at the rate of 200 μl. The results revealed that cytokine level of interleukin-1 beta (IL-1 β ) and tumor necrosis factor alpha (TNFα) in serum was reduced in TQ-treated rats. Immunohistochemical study showed that expression of NF-kB was countered in the lung tissue by the application of TQ. In addition, the lesion score for various pathological aberrations were checked when rats were treated with TQ. From the results of the present study, it was concluded that TQ has an ameliorative effect on the pulmonary blood vascular damage via rearrangement of the cytokines in response to LPS injury in the rat model.