ACETAMINOPHEN (PARACETAMOL)

Mechanism of Action-Prostaglandin’s synthesis is weakly inhibited like selective cyclooxygenase-2 inhibitors and also decreased concentration of prostaglandins.

Reason of toxicity -Deficient in glucuronidation and sulfation abilities, N-acetyl- p- benzoquinoneimin e (NAPQI) formed alternatively bind and damage the hepatic cell membrane leading to its injury and death subsequently 

ASPIRIN

Mechanism of Action-Cyclooxygenase e nzyme inactivation irreversibly leads to suppression of the thromboxanes & prostaglandins.

Reason of toxicity - Less of glucuronyl transferase and glycine conjugation

SALICYLATES 

Mechanism of Action- Nonselective inhibition of peripherally and centrally mediated cyclooxygenase. Potent inhibitor of thromboxane production function.

Reason of toxicity- Relatively deficient in glucuronosyl transferase, which conjugates salicylate with glucuronic acid.

IBUPROFEN, CARPROFEN, ETODOLAC

Mechanism of Action- Inhibition of cyclooxygenase activity, blocking the production of prostaglandins, substances that the body releases in response to illness and injury.

Reason of toxicity-Low capacity for hepatic glucuronidation, needed for elimination.

MELOXICAM, PIROXICAM

Mechanism of Action-Preferential inhibition of COX-2 and sparing COX-1 alone.

Reason of toxicity-Low capacity for hepatic glucuronidation, needed for elimination.

APRAMYCIN

Mechanism of Action-Inhibition of microbial protein synthesis accomplished through binding to the bacterial 30S small ribosomal subunits

Reason of toxicity -These drugs are concentrated in the labyrinthine fluid and vestibular/cochlea r sensory cells and hairs undergo concentration dependent destructive changes.

CHLORAMPHENICOL

Mechanism of Action-Inhibition of microbial protein synthesis accomplished through reversibly binding to the 50S subunit of the bacterial ribosome and inhibition of the peptidyl transferase step of protein synthesis.

Reason of toxicity -Needs to be metabolized in liver as Chloramphenicol glucuronide

AMITRAZ

Mechanism of Action-Activates alpha-2 adrenergic receptor in the central nervous system (CNS), alpha2 and alpha1 adrenergic receptor in the peripheral nervous system (PNS).

Reason of toxicity -Stimulation of α2- adrenergic receptors that generates the main signs of amitraz poisoning, such as loss of consciousness, breathing depression, seizures, bradycardia, hypotension, and hypothermia

PYRETHRINS & PYRETHROID

Mechanism of Action-Axonic excitotoxins, the toxic effects of which are mediated through preventing the closure of the voltage-gated sodium channels in the axonal membranes in muscle and nervous tissue

Reason of toxicity -Lack of the metabolising enzyme glucuronosyl transferase

SALINOMYCIN

Mechanism of Action-Inhibition of ookinete development, oocyst formation in the mosquito midgut, blocking their transmission Selectively damages infected erythrocytes.

Reason of toxicity-Polyneuropathy of the peripheral nerves, characterized by primary axonal degeneration and secondary degeneration of the myelin sheath resulting in paralysis. hypoxia of the myocardium due to dyspnoea from paralysis of the respiratory musculature

BENZOCAINE

Mechanism of Action-Stabilizes the neuronal membrane reversibly, decreasing its permeability to sodium ions, inhibition of depolarization of the neuronal membrane blocking of initiation and conduction of nerve impulses.

Reason of toxicity -Due to their unique hemoglobin structure, it is easily damaged

PROPOFOL

Mechanism of Action-Decreases the rate of dissociation of the Gamma- aminobutyric acid (GABA) from the receptor, duration of the GABA- activated opening of the chloride channel increased resulting hyperpolarization of cell membranes.

Reason of toxicity -Lack of glucuronosyl transferase which is needed to glucuronidate propofol.