Journal of Applied Toxicology

Ghrelin is a novel brain–gut peptide that plays various roles in mammals, including control of food intake and growth hormone release, as well as gastric motility and acid secretion in the gastrointestinal tract. Evidence exists supporting ghrelin's antiapoptotic actions and its protective effects against drug-induced toxicity and ischemia–reperfusion injury in different organs. In the current review, the available regarding ghrelin and its effects on different modes of target tissue injury are summarized.

The endocannabinoid system and especially its ligands, the endocanabinoids, have received increasing attention as potential neuroprotective agents against chemical-induced injury and other adverse effects. Endocannabinoids serve as retrograde signalling messengers in GABAergic and glutamatergic synapses, as well as modulators of post-synaptic transmission, interacting with other neurotransmitters, including norepinephrine and dopamine. Furthermore, they exert neuromodulatory, anti-excitotoxic, anti-inflammatory and vasodilatory effects. We present here recent data regarding the protecting role of endocannabinoids in cases of neurotoxicity.

MCF-7 BOS human breast cancer cells were used to investigate the potential for cytotoxicity, estrogenicity, and anti-estrogenicity of triclosan, PFOS, and PFOA at environmentally relevant concentrations. Results revealed that both triclosan and PFOA were cytotoxic while PFOS showed no significant cytotoxicity. E-SCREEN testing revealed positive estrogenic activity by all contaminants. Significant anti-estrogenic activity was detected for all compounds when cells were co-exposed with estradiol. The results demonstrated that these contaminants have estrogenic activities and co-exposure with estradiol produced anti-estrogenic effects.

We investigated the positional preference for sulfation and glucuronidation of seven structurally similar flavones in vitro and in situ. Flavone glucuronidation and sulfation rates were sensitive to minor changes in molecular structure. In intestinal S9 fractions, both Ugts and Sults preferentially catalyzed reactions at 7-OH. The sulfation rate was significantly enhanced by simultaneous glucuronidation, but glucuronidation was unaltered by sulfation.Sulfation rates in mouse S9 fractions correlated with sulfation rates in perfused intestine.

The possibility of DNA damage in sputum cells was examined in 56 premenopausal women who cooked with biomass and 49 matched control who cooked with cleaner fuel. DNA damage was upregulated in biomass users in association with elevated level of urinary t,t-MA, increased ROS generation and depleted SOD along with elevated PM₁₀ and PM_2.5 in cooking areas. Thus, biomass smoke causes DNA damage in airway cells, possibly by oxidative stress generated by inhaled pollutants including PM and benzene.

The goal of this study was to develop and validate a simple assay for measuring acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) activities in whole blood from humans as well as experimental animals. AChE activity was determined by measuring the hydrolysis of acetylthiocholine in the presence of 20 µ m ethopropazine and BChE activity was determined by measuring the hydrolysis of butyrylthiocholine in the absence of an inhibitor. The method was validated for blood from several animal species, including rodents and nonhuman primates.

Rats were exposed to crystalline silica and global gene expression profile was determined in the lungs at post-exposure time intervals. The number of significantly differentially expressed genesin the rat lungs correlated with silica-induced pulmonary toxicity. Genes involved in oxidative stress, inflammation, respiratory diseases, cancer, and tissue remodeling and fibrosis were significantly differentially expressed in the lungs. Collectively, the findings of our study provided insights into the molecular mechanisms underlying the progression of crystalline silica-induced pulmonary toxicity in the rat.