Carbaryl stress induced cellular changes in Calothrix brevissima

Abstract

Cyanobacterial biofertilizers are affected by paddy field pesticides as nontarget organism. Carbaryl is a carbamate pesticide and is commonly used against rice thrip pest in paddy fields. In the present work, cellular changes caused by exposure of the cyanobacterial biofertilizer namely Calothrix brevissima to carbaryl were studied with special reference to fatty acids, electrolyte leakage, sulfur metabolism, and osmolytes. To study the toxic effect of carbaryl, the test cyanobacterium was exposed to varying concentrations of pesticide (0, 10, 20, 30, and 40 mg L(-1)) for biochemical analyses. At 40 mg L(-1) carbaryl, polyunsaturated fatty acids were reduced by 32 % and membrane leakage was increased by 27 % suggesting that free radical-mediated lipid peroxidation took place. The sulfur-containing metabolites namely cysteine, cystine, and methionine were increased by 79, 64, and 52 %, respectively. The enzymatic and nonenzymatic antioxidants namely glutathione S-transferase, glutathione reductase, reduced glutathione, and oxidized glutathione were increased to 56, 71, 72, and 60 %, respectively. Osmolytes that serve as stress enzyme protectors as well as nonenzymatic free radical scavenger were also increased, indicating their protective nature in context with carbaryl-induced stress. The respective increase in mannitol, trehalose, and glycogen were 158, 98, and 159 %. In C. brevissima, carbaryl-induced membrane leakage was counteracted by increasing enzymatic and nonenzymatic parameters that helped in scavenging free radicals.

Carbaryl-induced ototoxicity in rat postnatal cochlear organotypic cultures

“…Carbaryl also disrupts melatonin synthesis and secretion in the pineal gland (Attia et al, ), but the long term health consequences of this are unclear. Some reports indicate that carbaryl induces oxidative stress and membrane leakage suggestive of lipid peroxidation; these changes were associated with increases in free radical scavengers, upregulation of stress genes and DNA repair genes (Delescluse et al, ; Slaninova et al, ; Geret et al, ; Habib et al, ). Others have found that carbaryl inhibits mitochondrial respiration and the mitochondrial membrane potential; however, these changes only occurred at high concentrations suggesting that they were secondary effects (Moreno et al, ).…”