Oxidative stress resulting from the disproportion of oxidants and antioxidants contributes to both physiological and pathological conditions in sepsis. To combat this, the antioxidant defense system comes into the picture, which contributes to limiting the amount of reactive oxygen species (ROS) leading to the reduction of oxidative stress. However, a strong relationship has been found between scavengers of ROS and antioxidants in preclinical in vitro and in vivo models. ROS is widely believed to cause human pathology most specifically in sepsis, where a small increase in ROS levels activates signaling pathways to initiate biological processes. An inclusive understanding of the effects of ROS scavenging in cellular antioxidant signaling is essentially lacking in sepsis. This review compiles the mechanisms of ROS scavenging as well as oxidative damage in sepsis, as well as antioxidants as a potent therapeutic. Direct interaction between ROS and cellular pathways greatly affects sepsis, but such interaction does not provide the explanation behind diverse biological outcomes. Animal models of sepsis and a number of clinical trials with septic patients exploring the efficiency of antioxidants in sepsis are reviewed. In line with this, both enzymatic and non-enzymatic antioxidants were effective, and results from recent studies are promising. The usage of these potent antioxidants in sepsis patients would greatly impact the field of medicine.

Extracellular vesicles (EVs) are nanosized vesicles released by different cells and have been separated from most of the body fluids. These vesicles play a central role in cell-to-cell communications as carry a distinct cargo including proteins, RNA species, DNAs, and lipids that are meant to be shipped and exchanged between cells at both systemic and paracrine levels. They serve in regulating normal physiological processes. EVs released from stem cells exert similar therapeutic effect to their originating cells. Clinical application of EVs requires the preparation of sufficient and viable active therapeutic EVs as well as implementing suitable methods for long-term preservation to expedite both their clinical and commercial uses. Cryopreservation is the most common method used to preserve decomposable biomaterials. However, cryopreservation causes cryoinjury to cells which therefore necessitate the use of cryoprotectants. Two types of cryoprotectants exist: penetrating and non-penetrating. In freeze drying, the watery content is sublimed from the product after it is frozen. This drying process is pertinent to thermo-liable substances and those unstable in aqueous solutions for prolonged storage periods. In spray drying technique, the solution containing EVs is firstly atomized, then droplets are rapidly converted into a dry powder using heated gas. Even with the exposure to high temperatures of the drying gas, spray drying is considered suitable for heat-sensitive materials. EVs are considered a promising cell-free therapy, but the lack of proper preservation limits its benefits. Preservation of EVs will initiate a vast amount of clinical trials on different species and different clinical problems.

1. Florfenicol (30 mg/kg body weight) was administered to broiler chickens via intravenous (iv), intramuscular (im) and oral routes to study its plasma concentrations, kinetic behaviour, systemic bioavailability and tissue content. 2. Following a single iv injection, the kinetic disposition of florfenicol followed a 2‐compartmental open model with an elimination half‐life of 173 min, total body clearance of 26.9 ml/kg/min and a steady state volume of distribution of 5.11 1/kg. 3. The highest plasma concentrations of florfenicol were 3.82 and 3.20 μg/ml following single im and oral administration, respectively. The systemic bioavailability was 96.6% and 55.3% after im and oral administration. The plasma protein binding of florfenicol was 18.5%. 4. Following its administration, the highest tissue concentrations of the drug were found in the kidney bile, lung, muscle, intestine, heart, liver, spleen and plasma. Low concentrations of the drug were found in brain, bone marrow and fat. No florfenicol residues were detected in tissues and plasma after 72 h except in the bile from where it disappeared after 96 h.