Scrutinizing impact of atrazine on stress biomarker: plasma glucose concentration of fresh water fish, grass carp, (Ctenopharyngodon idella)

Abstract

Herbicide praxis in agricultural fields to curb herbs is utterly toxic to non-target areas like aquatic bodies and impinge aquatic organism distinctively fish health through impairment of metabolism, sometimes leading to mortality. Therefore to contemplate the acute (short term) and chronic (long term) toxicological effects of atrazine, study was designed to scrutinize the potential detrimental effects of commercial utilization of chemical named; atrazine,  on aquatic organisms through evaluating stress biomarker; plasma glucose (energy currency) of freshwater fish; grass carp, (Ctenopharyngodon idella)for 01(24), 02(48), 03(72), 04(96), 10(240), 15(360) and 15(600) days(hrs) under the dose 15µl/L, 13µl/L, 10µl/L and 08µl/L, 06µl/L, 04µl/L, 02µl/L respectively. For analysis of plasma glucose concentration the protocol haematological analyzer (Mindray BC-2300 Hematology Analyzer) was followed in the laboratory. Above 15µl/L LC₅₀ was recorded indicating grass carp sensitivity to atrazine. Control plasma glucose concentration was 42.3mmol/L. Paramount downturn during acute toxicity and chronic toxicity was observed after 01 day (24hrs/15µl/L) and 10 days (240hrs /06µl/L) exposure respectively among treated groups while in both groups with the declining of dose quantity an inclined in glucose concentration was observed. Downturn in concentration indicating the toxicity of atrazine to liver and upturn in concentration may be due to enhancing glycogen breakdown in the liver and consequently elevates blood glucose level in response of stress to cope with new environmental conditions. Our study is also purposive to fathom that atrazine is causing agent of acute and chronic health problem to aquatic organisms and induced stress in fish body which revealed pessimistic domination on ecosystem of the aquatic organisms.

Keywords: Atrazine; Plasma glucose; Acute toxicity; Chronic toxicity; Biochemical

http://dx.doi.org/10.19045/bspab.2017.600141