Biochemical effects of diquat and paraquat. Disturbance of the control of corticosteroid synthesis in rat adrenal and subsequent effects on the control of liver glycogen utilization

Abstract

1. Administration of diquat (NN'-ethylene-2,2'-bipyridilium) or paraquat (NN'-dimethyl-4,4'-bipyridilium) prevents the normal depletion of liver glycogen in starved rats. 2. There is an increase in blood glucose, which returns to normal values after approx. 7h. 3. After administration of diquat or paraquat, plasma corticosteroids increase to very high concentrations and remain high for at least 24h, but plasma ACTH (adrenocorticotrophin) is only increased for 4h. 4. Adrenal cyclic AMP is considerably increased after administration of diquat and remains significantly higher than control values for at least 24h. 5. It is suggested that diquat and paraquat increase the response of the adrenal cortex to ACTH.

Acute paraquat exposure determines dose‐dependent oxidative injury of multiple organs and metabolic dysfunction in rats: impact on exercise tolerance

“…Although the influence of PQ on glucose metabolism has been described (Rose et al . ; Giri et al . , ), this effect is still not completely understood.…”

Effect of Bark Extract of Bathysa cuspidata on Hepatic Oxidative Damage and Blood Glucose Kinetics in Rats Exposed to Paraquat

“…The dose of 400 mg of the extract was sufficient to reduce the variation of blood glucose levels and prevent the PQ-induced depletion of liver glycogen. Although few studies exist in this area, the effect of PQ on glucose metabolism has been described in mammals, including rats (Giri et al 1979;Giri et al 1983;Rose et al 1974). This effect has yet to be fully explained; however, high levels of circulating catecholamines and corticosteroids have been identified in the initial phases of PQ poisoning (twenty-four hours) and are often associated with marked glycogenolysis, gluconeogenesis, and depletion of liver glycogen reserves (Giri et al 1979;Konstantinova and Russanov 1999;Suntres 2002).…”

“…This effect has yet to be fully explained; however, high levels of circulating catecholamines and corticosteroids have been identified in the initial phases of PQ poisoning (twenty-four hours) and are often associated with marked glycogenolysis, gluconeogenesis, and depletion of liver glycogen reserves (Giri et al 1979;Konstantinova and Russanov 1999;Suntres 2002). It is believed that the high levels of catecholamines and corticosteroids in PQ poisoning are a result of oxidative damage to the cortex and medulla of the adrenal gland (Giri et al 1979;Rose et al 1974). Thus, this mechanism would justify the use of antioxidant compounds in the prevention of glucose metabolism disorders related to these hormones in PQ poisoning. )…”

Effect of diquat on cell growth and macromolecule synthesis in cultured pneumocytes.

“…It is presumed that DQ produces metabolic disturbances, such as an increase of glucose utelization in the liver of that of cyclic AMP in the adrenal gland of the (Rose et al 1974) and depletion of NADPH in the lung of the rat (Witschi et al 1977). In the present study, it was demonstrated that DQ has an inhibitory effect on cell growth.…”

“…DQ has been said to affect cyclic AMP, ACTH or glucose level of rat (Rose et al 1974), but the biological effects underlying the mammalian toxicity of DQ are not fully understood. Once DQ has been suggested to be accumulated into cultured pneumocytes (Saito and Menzel 1979), and the cells used in the present study have been shown to be sensitive to the toxicity of paraquat (PQ), another bipyridilium herbicide related to DQ (Saito 1985 (Lieber et al 1976) and human embryonic lung fibroblast cells (HEL) (Peterson et al 1978), were obtained from American Type Culture Collection (Rockville, MD, USA).…”