Priming dose of phenylhydrazine protects against hemolytic and lethal effects of 2-butoxyethanol

Palkar, Prajakta S.; Philip, Binu K.; Reddy, Ramesh N.; Mehendale, Harihara M.

doi:10.1016/j.taap.2007.06.011

Cited by 4 publications

(1 citation statement)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1,2 A well-known example of autoprotection is that of CCl 4 autoprotection. 3,4 Well-known examples of heteroprotection are the protection provided by the priming dose of thioacetamide (TA) against a lethal dose of acetaminophen (APAP) in male Sprague Dawley (SD) rats, 2 phenylhydrazine against 2-butoxyethanol-induced hematotoxicity in female SD rats, 5 and by mercuric chloride (HgCl 2 ) against S -(1,2-dichlorovinyl)- l -cysteine-induced nephrotoxicity in mice. 6 This previous work revealed that sustained compensatory tissue repair (CTR), induced by a priming dose of a toxicant, underlies the auto- and heteroprotection phenomena.…”

Section: Introductionmentioning

confidence: 99%

Hepatic Overexpression of Annexin A1 and A2 in Thioacetamide-Primed Mice Protects Them Against Acetaminophen-Induced Liver Failure and Death

et al. 2016

Self Cite

View full text Add to dashboard Cite

Compensatory tissue repair (CTR) in thioacetamide (TA)-primed rats protects them against acetaminophen (APAP)-induced lethality. This study was aimed at investigating the mechanisms of CTR-mediated heteroprotection in mice. Male Swiss Webster mice received a priming dose of TA (40 mg/kg body weight [BW] in 10 mL distilled water [DW]/kg BW, intraperitoneally [IP]). Thioacetamide-induced liver injury, CTR, and expression of annexin A1 and A2 (ANX1 and ANX2), the endogenous inhibitors of the death protein secretory phospholipase A2 (sPLA), were measured over a time course of 84 hours after TA priming. Both centrilobular necrosis and CTR peaked at 36 hours after TA priming as indicated by significantly increased plasma alanine transaminase (ALT) and aspartate transaminase (AST) activities, liver histology, and proliferating cell nuclear antigen immunostaining. Thioacetamide priming resulted in the overexpression of ANX1 and ANX2 at 36 to 84 hours and 12 to 60 hours, respectively. A lethal dose of APAP (600 mg/kg BW in 10 mL 0.45% NaCl/kg BW, IP) was given at 12, 24, or 36 hours after TA-priming. Thioacetamide priming did not affect the rise in plasma ALT, AST, sPLA, and arachidonic acid levels seen at 2 hours after the APAP overdose. Neither these biochemical parameters nor histology suggested any escalation of hepatic injury at later time points (12 and 24 hours after APAP overdose), consistent with 100% survival of the TA + APAP-treated mice compared to DW + APAP-treated mice, which had 100% mortality. Inhibition of ANX1 and ANX2 biosynthesis using cycloheximide (40 mg/kg BW in 5 mL DW/kg BW, IP) abolished this heteroprotection. Our data indicate that hepatic overexpression of ANX1 and ANX2 inhibits APAP-induced expansion of liver injury.

show abstract

Section: Introductionmentioning

confidence: 99%

Hepatic Overexpression of Annexin A1 and A2 in Thioacetamide-Primed Mice Protects Them Against Acetaminophen-Induced Liver Failure and Death

et al. 2016

Self Cite

View full text Add to dashboard Cite

show abstract

Ethers of Ethylene Glycol and Derivatives

Kelsey

2023

Patty's Toxicology

View full text Add to dashboard Cite

E series Glycol ethers are alkyl ethers of ethylene glycol along with their acetate esters. They are commonly used in paints and cleaners and typically have a higher boiling point in conjunction with the favorable solvent properties of lower‐molecular weight ethers, esters, and alcohols. They are colorless liquids that have mild earthy or fruity odors. The ethers are miscible with water and/or with numerous organic solvents making them useful as solvents in oil‐water compositions. Their relatively slow rate of evaporation also makes them useful as solvents and coalescing agents in paints and inks. The surface tension and solvent properties of the ethers make them useful in cleaners. Other uses of the ethers include process solvents and deicers. The ethers of the higher glycols are used as hydraulic fluids. Occupational exposure to glycol ethers occurs dermally and by inhalation. Most glycol ethers have low acute, single‐dose toxicity to humans. The most notable and well‐known effect relevant to humans is toxicity to male fertility and developmental toxicity produced by those glycol ethers that can metabolize to produce significant amounts of methoxyacetic acid such as methoxy ethanol and the methyl glymes.

show abstract

Ethers of Ethylene Glycol and Derivatives

Cragg¹

2012

Patty's Toxicology

View full text Add to dashboard Cite

There are seven U.S. manufacturers of ethers and other derivatives of ethylene glycol (EG), diethylene glycol (DEG), and higher glycols. Five of them are members of the American Chemistry Council (ACC) Glycol Ethers' Panel. The glycol ethers most commonly encountered industrially are colorless liquids that have mild ethereal odors. Alkyl glycol ethers are manufactured in a closed, continuous process by reacting ethylene oxide with an anhydrous alcohol in the presence of a suitable catalyst. Depending on the molar ratios of the reactants and other process parameters, the product mixtures obtained contain varying amounts of the monoethylene, diethylene, triethylene, and higher glycol ethers. Typically, the products in these mixtures are separated and purified by fractional distillation. The miscibility of most of these ethers with water and with a large number of organic solvents makes them especially useful as solvents in oil–water compositions. Their relatively slow rate of evaporation also makes them useful as solvents and coalescing agents in paints. Other uses include inks, cleaners, chemical intermediates, process solvents, brake fluids, and deicers. The ethers of the higher glycols are used as hydraulic fluids. An estimate of the U.S. production and use of representative ethylene glycol ethers is presented. Production of ethylene glycol ethers (total) in Western Europe amounted to 245 thousand metric tons in 1995. Occupational exposure to glycol ethers occurs dermally and by inhalation. Ingestion is not a concern in industrial exposure, although some cases of intentional ingestion of consumer products containing ethylene glycol ethers have been reported. A number of analytical methods have been published that are suitable for detecting glycol ethers in environmental air samples. Glycol ethers generally have low acute, single‐dose toxicity, and LD 50 values generally range from 1.0 to 4.0 g/kg of body weight. In animals and humans, high‐dose administrations (>350 mg/kg) result in central nervous system (CNS) depression, although the results from many studies show no specific damage to neural tissues. Other toxicological effects attributable to glycol ethers are associated with metabolism to the corresponding alkoxyacetic acids. In the case of EGME, EGEE, and certain other glycol ether derivatives, significant reproductive, developmental, hematologic, and immunologic effects have been associated with the formation of either methoxyacetic acid (MAA) or ethoxyacetic acids (EAA). For other glycol ether derivatives substituted with propyl, butyl, or higher homologues, both developmental effects secondary to maternal toxicity (without teratogenic effects) and hematologic effects are observed. Ethylene glycol ethers and acetates may enter the environment from manufacturing effluents and emissions and as a result of their use in commercial products.

show abstract

Priming dose of phenylhydrazine protects against hemolytic and lethal effects of 2-butoxyethanol

Cited by 4 publications

References 44 publications

Hepatic Overexpression of Annexin A1 and A2 in Thioacetamide-Primed Mice Protects Them Against Acetaminophen-Induced Liver Failure and Death

Hepatic Overexpression of Annexin A1 and A2 in Thioacetamide-Primed Mice Protects Them Against Acetaminophen-Induced Liver Failure and Death

Ethers of Ethylene Glycol and Derivatives

Ethers of Ethylene Glycol and Derivatives

Contact Info

Product

Resources

About