Determination of Median Lethal Concentration (LC50) and Nitrite Accumulation in the Blood and Tissue of Blood Cockle (Tegillarca granosa, Linnaeus 1758)

Nurul Hazwani Hashim,Zulfa Hanan Asha’Ari,Ferdaus Mohamat-Yusuff,Amirul Azuan Joni,Syaizwan Zahmir Zulkifli,Zufarzaana Zulkeflee,Faradiella Mohd Kusin,Khairul Nizam Mohamed

doi:10.3390/w12082197

Abstract

This study aimed to determine the nitrite toxicity of blood cockle Tegillarca granosa, with the objectives being to identify the median lethal concentration (LC50) and the accumulation level of nitrite in Tegillarca granosa, and to determine the relationship of nitrite accumulation with mortality percentage. The levels of LC50 and accumulation of nitrite were determined after 72 h of exposure to different nitrite concentrations (0, 0.5, 1.0, 1.5, and 2.0 mg/L). Nitrite accumulation was analysed using Method 8153 and a DR2800 spectrophotometer (HACH, Loveland, CO, USA). LC50 was identified at 1.53 mg/L, and nitrite accumulated in the ranges of 0.012 to 0.106 mg/L wet weight and 0.002 to 0.089 mg/L wet weight in the blood and soft tissue samples, respectively. Accumulation concentration in both tissue and blood cells increased proportionally with the exposure concentration, and had a strong positive relationship with the percentage of mortality. Our findings suggest that prolonged exposure of nitrite led to accumulation in the blood and tissues and caused cockle mortality.

Highlights

The presence of high nutrient residue in aquatic environments has been known to harm receiving water bodies
The median lethal concentration (LC50) of nitrite in blood cockles was calculated to be 1.53 mg/L based on Probit analysis, and the 95% confident interval was between
No significant differences were found for nitrite concentration in blood and awet highsoft level of MetHb suffer anemia, owing to the of that the total tissue samples at functional each concentration exposure

Summary

Introduction

The presence of high nutrient residue in aquatic environments has been known to harm receiving water bodies. The presence of nutrient byproducts in water may cause aquatic life mortality. The presence of nitrite (NO2 − ) due to the reduction of nitrates under conditions of an oxygen deficit increases the risk of accumulation of toxic nitrite, and may result in mass aquatic life mortality [1,2]. Nitrite has resulted in the inhibition of chloride ion uptake at the bronchi, impairment of the acid–base balance and the electrolyte balance, reduction of the oxygen-carrying capacity of blood by the oxidation of haemoglobin (Hb) to methaemoglobin

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