acetaminophen

In recent years anti-virulence agents have been used widely to reduce bacterial resistance and prevent damage to host cells and normal flora.  Six  molecules were used in this study (according to previous in silico studies) to detect their antibiofilm activity in lab. Four molecules gave positive results and were as follows : Acetaminophen inhibited biofilm production 100% at 11000µg/ml concentration, Acetylsalicylic Acid inhibition was 100% at 1600µg/ml , Ibuprofen inhibited 35% of biofilm production at 600µg/ml and Acetic Acid inhibition was 25% at 1000 µg/ml concentration .All the molecules at the used concentrations were found to affect biofilm production without significant change in bacterial growth. It was concluded that a structure based drug design strategy using Ligand Based Virtual Screening had a success score of about 60% and that Acetaminophen, Acetylsalicylic Acid, Ibuprofen and Acetic Acid can be used as antibiofilm molecules . Also Non-Steroidal Anti-Inflammatory Drugs family can be a useful library for antibiofilm future investigations.

Autism Spectrum Disorder (ASD) represents a major public health concern as a prevalent neurodevelopmental disorder with pronounced risk for failure of adaptation across social, educational, and psychological outcomes. The exact etiology of autism is unclear. However there is a lot of research work giving some insights about the possible predisposing factors that enhance chance of autism. Several lines of evidence suggest that prenatal and/or early life acetaminophen exposure may adversely affect neurodevelopment increasing incidence of autism. Since 1980 acetaminophen greatly has replaced aspirin as an analgesic and anti-pyretic following reports indicating that aspirin use was associated with Reye’s syndrome. Notably acetaminophen use has been associated with at least a 10-fold rise of autism epidemic since the early 1980s. Several mechanisms have been suggested to implicate the role of acetaminophen in pathogenesis of autism as altered immune function and impaired hepatic detoxification capacity resulting in accumulation of potentially neurotoxic metabolites. In early life, maturational compromises to the glucuronidation pathway in combination with the compromises to the sulfation pathway that typify autistic children, may lead to utilization of the suboptimal secondary metabolic routes with the potential for adverse neurological effects in susceptible individuals. Acetaminophen use during pregnancy has also been associated with altered metabolism increasing autism rates in born infants. The use of acetaminophen may also trigger autism by activating the endocannabinoid system thereby interfering with normal development. Accumulating evidence linking significantly increased rates of autism with prenatal and early life acetaminophen exposure strongly suggests its cautious use during these critical times.