EVALUATION OF THE CHRONIC EFFECT OF NITRATE AND RECOVERY THROUGH COMPENSATORY GROWTH IN THE PACIFIC WHITE SHRIMP Litopenaeus vannamei IN BIOFLOC TECHNOLOGY SYSTEM

Introduction

The development of new technologies for aquaculture systems is essential to reach economic, social and environmental sustainability and allow the continuously growth of aquaculture production.  In this scenario, the Biofloc Technology System (BFT) have been considered one of the possible solutions and opportunities to further develop aquaculture. However, one of the concerns in the BFT systems is the nitrate accumulation during the culture period, due to zero or low water exchange during the culture period and the constant reuse of water. Therefore, the present work aimed to evaluate the chronic stress of nitrate in L. vannamei and the possible recovery of growth rates when  nitrate low levels are re-established through compensatory growth, which is defined as a physiological process where the organism goes through a rapid phase of growth after a restricted period of development.

Material and methods

The present work was divided in two experiments. Firstly, a Lethal Concentration 50 (LC50- 96h) was conducted in clear water to define the nitrate safe level for L.vannamei in salinity 25 mg., calculated using the Trimmed Spearman-Karber Method. Therefore, Nine concentrations of nitrate were chosen to the lethal test: zero (control), 1000, 1500, 2000, 2500, 3000, 3500, 4000 and 4500 mg.of N- NO₃.

From the result obtained from the lethal test, the chronic experiment was conducted in BFT. Thus, L. vannamei juveniles were stocked with an initial weight of 0.82 g (± 0.25 g) at a stocking density of 300 shrimps/m³.The experiment was performed using a 3 × 2 experimental design (two nitrate concentrations and three exposure time), plus the control (which the nitrate level was maintained lower than 20% of the safe level),totaling seven treatments (in triplicate) and lasted 58 days. The experiment was divided into two phases: (1) Stress and (2) Recovery. Two nitrate concentrations were chosen (safe level determined in the first experiment and half-safe level - 278.91 and 139.45, respectively) and three exposure times were established for each nitrate concentration (10, 20 and 30 days). After the stress period, which varied according to the treatment, the experimental units were exposed to optimum conditions until the experiment complete 58 days.

The treatments exposed to half of the safe level and the groups that were submitted to the nitrate safe level limit during 10, 20 and 30 days  were named as 0.5*SL - 10, 0.5*SL - 20 and 0.5*SL - 30, 1.0*SL -10, 1.0*SL - 20 and 1.0*SL – 30, respectively.

Results and discussion

From the lethal test, the estimated LC50-96h was 2789.11, and safe level was determined through Sprague Factor (0.1 of the LC50-96h). Regarding the chronic experiment, survival did not present any difference among treatments over the experimental period. At the end of the stresses phases (day 10, 20 and 30), the weight, Weekly Growth Rate (WGR) and Specific Growth Rate (SGR), of the treatments submitted to 0.5 and 1.0 times of the nitrate safe level during 10 and 20 days (0.5*SL – 10, 0.5*SL - 20, 1.0*SL -10, 1.0*SL – 20) did not statistically differ from the control group. However, after 10 days (day 30) of recovery, in the treatments submitted to 20 days of stress (0.5*SL – 20, 1.0*SL – 20), a statistical difference was found between both treatments and the control. Regarding the treatment exposed to 0.5 times the safe level for 30 days (0.5*SL – 30), it did not present differences compared to the control treatment on day 30, while the treatment exposed to the safe limit level during 30 days (1.0*SL – 30) presented a lower weight compared to the control group. At day 40, the control statistically differ from the treatments stressed during 30 days (0.5*SL – 30, 1.0*SL – 30), which did not differ between them. The  Apparent Feed Converstion Rate (AFCR) from the stressed groups during 10 and 20 days did not differ from the control group. Despite that, both 0.5*SL – 30 and 1.0*SL – 30 treatments presented higher AFCR compared to the control group.

After the end of the recovery phase (day 58), no significant differences were found in the body mass among treatments. In addition, no differences were found in the WGR and SGR among treatments previous stressed during 10 and 20 days and the control group. The treatment 1.0*SL – 30 presented higher WGR compared to the control treatment and did not differ from the 0.5*SL – 30. SGR also had an also rate in the 1.0*SL – 30 treatment, followed the 0.5*SL – 30 group, while the control presented the lower SGR.   AFCR did not present statistical differences among control and both groups exposed to high nitrate levels during 10 days.  Regarding to treatments previous stressed during 20 and 30 days, the control group presented higher AFCE compared to the 0.5*SL – 20 and 0.5*SL-30 treatments, and did not differ from 1.0*SL – 20 and 1.0*SL – 30 groups. 

Despite the depressed growth after the nitrate exposure in the treatments mentioned above, the animals were able to recovery the growth rates when exposed to lower levels of nitrate, characterizing total compensatory growth in all treatments previously affected by the high nitrate concentration.

CG is usually evaluated through the improvement of SGR and the feed conversion rate in the stressed treatments compared to the control after the recovery phase, which are both considered an adequate parameter to conclude the occurrence of CG. In the present study, the SGR at the end of the experiment of the 1*SL – 30 and 0.5*SL – 30 treatments, previous affected by the chronic exposition at day 30, was higher than the control, even though the feed conversion rate did not differ from the control. Therefore, since no survivor losses was identified and the final weight did not differ among treatments, it is possible to conclude the treatments previous affected by the nitrate toxicity reached the control treatment weight through CG.

Conclusion

Even though  L. vannamei presents a great resistance to nitrate exposure, long expositions (more than 20 days) in high nitrate concentrations can negatively affect the growth rates. However, when nitrate lower values are re-established, the animals are capable to regrow in high rates and compensate the weight through compensatory growth.