[Clinical, laboratory and morphological comparisons in cellular alteration under conditions of hypoxia].

Objective: To compare structural changes in tissues with clinical and laboratory parameters and immunohistochemical determination of proteins HIF1α, HIF2α, caspase-3 during cellular alteration under conditions of hypoxia in the liver and kidneys in an experiment on pigs.

Material And Methods: Laboratory parameters related to the state of gas exchange (decrease in partial pressure of arterial blood oxygen (PaO2), arterial blood saturation, lactate level, kidney function (creatinine, urea) and liver (ALT, AST, bilirubin) in 18 animals were analyzed in comparison with the results of a morphological study. Histological examination evaluated alterative and inflammatory tissue changes of varying severity, and also determined the expression of transcription factors HIF1α and HIF2α and a marker of apoptosis - caspase-3.

Lack of neuropathological changes in rats administered tedizolid phosphate for nine months.

Tedizolid, a novel oxazolidinone antibacterial, was administered to Long Evans rats by oral gavage once daily for up to 9 months at doses near the maximum tolerated dose (MTD) to evaluate for potential neurotoxicity. Mean plasma exposures of tedizolid at the low-, medium-, and high-dose levels (7.5, 15, and 30 mg/kg of body weight/day for males; 2.

Nonclinical and pharmacokinetic assessments to evaluate the potential of tedizolid and linezolid to affect mitochondrial function.

Prolonged treatment with the oxazolidinone linezolid is associated with myelosuppression, lactic acidosis, and neuropathies, toxicities likely caused by impairment of mitochondrial protein synthesis (MPS). To evaluate the potential of the novel oxazolidinone tedizolid to cause similar side effects, nonclinical and pharmacokinetic assessments were conducted. In isolated rat heart mitochondria, tedizolid inhibited MPS more potently than did linezolid (average [± standard error of the mean] 50% inhibitory concentration [IC50] for MPS of 0.

STP position paper: Recommended practices for sampling and processing the nervous system (brain, spinal cord, nerve, and eye) during nonclinical general toxicity studies.

The Society of Toxicologic Pathology charged a Nervous System Sampling Working Group with devising recommended practices to routinely screen the central nervous system (CNS) and peripheral nervous system (PNS) in Good Laboratory Practice-type nonclinical general toxicity studies. Brains should be weighed and trimmed similarly for all animals in a study. Certain structures should be sampled regularly: caudate/putamen, cerebellum, cerebral cortex, choroid plexus, eye (with optic nerve), hippocampus, hypothalamus, medulla oblongata, midbrain, nerve, olfactory bulb (rodents only), pons, spinal cord, and thalamus.

An oral developmental neurotoxicity study of decabromodiphenyl ether (DecaBDE) in rats.

Background: Decabromodiphenyl ether (DecaBDE; CASRN 1163-19-5) is a flame retardant used in a variety of manufactured products. A single oral dose of 20.1 mg/kg administered to mice on postnatal day 3 has been reported to alter motor activity at 2, 4, and 6 months of age.