Production of biodiesel from waste fish fat through ultrasound-assisted transesterification using petro-diesel as cosolvent and optimization of process parameters using response surface methodology.

Biodiesel is a highly promising and viable alternative to fossil-based diesel that also addresses the urgent need for effective waste management. It can be synthesized by the chemical modification of triglycerides sourced from vegetable origin, animal fat, or algal oil. The transesterification reaction is the preferred method of producing biodiesel. However, the non-miscibility of alcohol and oil layer causes excessive utilization of alcohol, catalyst, and a substantial reacting time and temperature. In the current investigation, transesterification of waste fish oil was performed with petro-diesel as cosolvent, under the influence of ultrasound energy. The combination of both techniques is a unique and efficient way to minimize the mass transfer limitations considerably and hence reduces the parameters of the reaction. It is also a sincere effort to comply with the principles of green chemistry. The optimum reaction conditions were obtained using response surface methodology (RSM) that were as follows: molar ratio of methanol to oil 9.09:1, catalyst concentration of 0.97 wt%, cosolvent concentration of 29.1 wt%, temperature 60.1℃, and a reacting time 30 min. Under these listed conditions, 98.1% biodiesel was achievable, which was in close agreement with the expected result. In addition, the cosolvent removal step from the crude biodiesel was also eliminated as it could be employed as a blended fuel in CI engines.

Increasing NO level regulates apoptosis and inflammation in macrophages after 2-chloroethyl ethyl sulphide challenge.

Generation of nitric oxide (NO) in cellular compartments acts in a redox-dependent manner to counteract oxidative stress either by directly acting as an antioxidant through scavenging superoxide anions (O2-), to form peroxynitrite (ONOO-) or acting as a signaling molecule, altering gene expression that triggers various physiological processes. However, the molecular mechanisms of macrophage activation and NO production leads to apoptosis and inflammation after 2-chloroethyl ethyl sulphide (CEES) exposure remains unclear. We showed that CEES exposure in macrophages increased the O2- production. Also CEES exposure transiently increases the NO production and ONOO- accumulation via expression of inducible NO synthase (iNOS). Simultaneously, CEES exposure caused a significant reduction in cellular antioxidants and modulate lipid peroxidation (LPO), and protein carbonylation (PC) reactions, which was correlated with the increased level of NO and ONOO- accumulation. Mechanistic studies showed the DNA damage, 8-oxoGDNA glycosylase (OGG1) down regulation and 8-hydroxydeoxyguanosine (8-OHdG) accumulations in DNA, which was also confirmed by phosphorylation of ATM, ATR and H2A.X. Elevated levels of NO/ONOO- plays an important role in apoptosis, and alteration of cell cycle regulatory proteins in macrophages after CEES exposure. Moreover, CEES exposure to macrophage cells enhanced the transcriptional activities of inflammatory mediators such as TNFα, IL-1α, ICAM, CX3CL1, CCL8, and CXCL10, which were linked with NO/ONOO- accumulation. These results showed a mechanistic explanation of how NO/ONOO- cooperate to conduct apoptosis and inflammatory signals in macrophages after CEES challenged. Further, the protective effects of NO/ONOO- inhibitors may provide the basis for the development of a therapeutic strategy to counteract exposure to CEES.