Antimicrobial uses for livestock production in developing countries.

Antimicrobial is an indispensable part of veterinary medicine used for the treatment and control of diseases as well as a growth promoter in livestock production. Frequent use of antimicrobials in veterinary practices may lead to the residue in animal originated products and creates some potential problems for human health. The presence of antimicrobial residues in animal originated foods may induce serious health problems such as allergic reaction, antimicrobial resistance (AMR), and lead to carcinogenic and mutagenic effects in the human body. The misuse or abuse of antibiotics in human medicine is thought to be a principal cause of AMR but some antimicrobial-resistant bacteria and their resistant genes originating from animals are also responsible for developing AMR. However, the residual effect of antimicrobials in feed and food products of animal origin is undeniable. In developing countries, the community is unaware of this residual effect due to lack of proper information about antibiotic usage, AMR surveillance, and residue monitoring system. It is imperative to reveal the current situation of antimicrobial use in livestock production and its impacts on public health. Moreover, the safety levels of animal feeds and food products of animal origin must be strictly monitored and public awareness should be developed against the indiscriminate use of antimicrobial in animal production. Therefore, the current review summarizes the literature on antimicrobial use in livestock production and its hazardous residual impacts on the human body in developing countries.

Development of a novel molecular probe for the detection of liver mitochondrial redox metabolism.

Redox status influences the course of the inflammatory, metabolic, and proliferative liver diseases. Oxidative stress is thought to play a crucial and sustained role in the pathological progression of early steatosis to severe hepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. Oxidative stress induced by reactive oxygen species which are generated in the mitochondria can lead to chronic organelle damage in hepatocytes. Currently, the diagnosis of liver disease requires liver biopsy, which is invasive and associated with complications. The present report describes the development of a novel molecular probe, EDA-PROXYL, with higher reactivity and mitochondrial selectivity than standard carboxyl-PROXYL and carbamoyl-PROXYL probes. The membrane permeability of our probe improved in aqueous environments which led to increased accumulation in the liver and interaction of EDA-PROXYL with the carnitine transporter via the amine (NH3+) group further increased accumulation. This increased mitochondrial sensitivity and enhanced accumulation highlight the potential of EDA-PROXYL as a molecular probe for determining metabolic reactions of the mitochondria. Thus, this novel probe could be a tool for the evaluation of redox status of the mitochondria to assess the degree of liver injury and, ultimately, the response to pharmacological therapy.

Synergy between phenotypic modulation and ROS neutralization in reduction of inflammatory response of hypoxic microglia by using phosphatidylserine and antioxidant containing liposomes.

Neuroinflammation caused by microglial activation is a key contributing factor in neurological disorders such as those involving ischaemia. Excess production of reactive oxygen species (ROS) and nitric oxide (NO) stimulates the inflammatory response during ischaemia, significantly damaging cells. Inhibition of inflammatory activation of microglia is a promising potential treatment approach for neurological diseases. In this study, we introduce α-tocopherol and phosphatidylserine (PS) containing liposomes (PST-liposomes) to inhibit the microglial inflammatory response. PS is known to have anti-inflammatory effects on microglia by modulating the microglial phenotype, while α-tocopherol is an antioxidant, known to neutralize ROS. We found that both PS-containing liposomes (PS-liposomes) and PST-liposomes, as compared with phosphatidylcholine containing liposomes, significantly increased viability of hypoxia-treated microglia. The PST-liposomes functioned better than the PS-liposomes and we attribute this superior effect to a synergy between PS and α-tocopherol. This synergic action of PST-liposomes was illustrated in their ability, when incubated with microglia, to reduce NO and pro-inflammatory cytokine (TNF-α) production and increase anti-inflammatory cytokine (TGF-ß1) production. Thus, the improved viability of hypoxia-treated microglia when treated with PST-liposomes involved anti-inflammatory effects, including ROS neutralization, as well as induction of a microglial phenotypic change. Our results suggest that PST-liposomes represent a potential therapeutic approach to reducing ischaemic injury in the brain.

Suppression of atopic dermatitis in mice model by reducing inflammation utilizing phosphatidylserine-coated biodegradable microparticles.

Controlling inflammatory response is important to avoid chronic inflammation in many diseases including atopic dermatitis (AD). In this research, we tried using a phosphatidylserine (PS)-coated microparticles in the AD mouse model for achieving the modulation of the macrophage phenotype to an anti-inflammatory state. Here, we prepared poly (D,L-lactic acid) microparticle coated with PS on the outside shell. We confirmed the cellular uptake of the PS-coated microparticle, which leads to the significant downregulation of the inflammatory cytokine production. In the mouse model of AD, the PS-coated microparticle was injected subcutaneously for a period of 12 days. The mice showed significant reduction in the development of AD symptoms comparing with the mice treated with the PC-coated microparticle.