## 3 Results
### Novel Tank Test
At 204 mg/L kojic acid, the severe toxic degeneration is represented by hepatocytes vacuolation, cell membranes fragmentation, and karyolysis (Figure 4B). At 284 mg/L kojic acid, due to severe/brutal toxic alteration, the hepatocytes appear disintegrated, with fragmented cell membranes (Figure 4C). Some hepatocytes show karyolysis or nuclear pycnosis. Figure 4: Kojic acid effects on the liver: (**A**) 100 mg/L; (**B**) 204 mg/L; (**C**) 284 mg/L. Vacuolation (\(\rightarrow\)), cell membrane fragmentation (\(\rightarrow\)), karyolysis/nuclear pycnosis (\(\rightarrow\)). Figure 3: Severe hepatocyte alteration. (**A**) Swollen hepatocytes with vacuolated cytoplasm and triglyceride loading; (**B**) Hydropic and lipidic dystrophy hepatocytes; hyperhydrated nucleus. The uniform degenerative appearance of the liver is translated by swollen hepatocytes, with fragmented membranes, but also cellular debris (nuclei, cell membranes, cytoplasmic blocks). The inflammatory component is absent. Patulin exposure leads to a medium-severe degeneration of urinary epithelium, swelling of the nephrocytes, cytoplasm vacuolation, nuclear hyperhydration (Figure 5A) while some nephrocytes lose integrity. The apoptosis of the renal cells was absent. Interstitial capillaries of the patulin-treated zebrafish are overloaded with erythrocytes, thus leading to a medium congestion. Due to a monocyte infiltration of the urinary epithelium, the patulin-treated zebrafish exhibit a renal inflammatory process. In the nephrocytes, we have observed the presence of large, vitreous casts (Figure 5B). The presence of increased numbers of hyaline casts can lead to kidney failure. The Hyalinosis presence in the tubular epithelium does not imply a nephrocyte lesion but the saturation of the physiological mechanism. Following exposure to 100 mg/L kojic acid, we have remarked a moderate degeneration of the proximal and distal urinary tract, noted by moderate alteration of the epithelium (Figure 6A). Nephrocytes are slightly swollen, have a granular cytoplasm, and the nuclei are hyperhydrated. Tubular lumens are slightly reduced. The 204 mg/L kojic acid dose leads to the degeneration of the proximal tubules nephrocytes, distinguished by granular, non-homogeneous cytoplasm and the presence of hyaline casts (Figure 6B). Hyalin denotes altered glomerular filtration, resulting in massive proteinuria. Hyalin is the result of intracytoplasmic accumulation of pinocyte proteins in the primary urinary filtrate. Figure 5: (**A**) degeneration of urinary epithelium: nephrocytes swelling, cytoplasm vacuolation, nuclear hyperhydration, interstitial capillaries congestion, monocyte infiltration of the urinary epithelium. (**B**) tubular cell hyaliosis. Figure 6: Effects of kojic acid on the kidneys: (**A**) 100 mg/L; (**B**) 204 mg/L; (**C**) 284 mg/L. Nephrocytes degeneration: granular cytoplasm (\(\rightarrow\)), hyaline casts (\(\rightarrow\)), swelling of the tubular epithelium, with tubular lumens disappearance (\(\rightarrow\)), prominent nucleoli (\(\rightarrow\)). The 284 mg/L kojic acid-treated group exhibits moderate kidney toxicosis: swelling of the tubular epithelium and tubular lumens disappearance (Figure 6C). The nephrocytes are swollen with abundant cytoplasm, hypertrophic nuclei and prominent nucleoli. Patulin exhibits toxic effects on the zebrafish heart, characterized by myocardial edema, enlarged interfibrillar spaces, swollen myocarditis and sarcoplasm hyperhydration (Figure 7). These effects can alter the cardiac function and lead to a decrease of the heartbeat rate. After 100 mg/L kojic acid exposure, we have noticed cardiac muscle fibers degeneration and perinuclear sarcoplasm vacuolization (Figure 8). There is also a moderate to severe myocardial congestion, characterized by ectasia and erythrocyte overload of the interstitial capillaries. At the beginning of analysis, the ANOVA test was used to compare the batch averages of variables present in the MAZE test.