Morphographic Changes in the Electrocardiogram of Colossoma macropomum Caused by Exposure to Manganese

Abstract

Manganese (Mn²⁺) is an abundant chemical element in the earth's crust and is present in soil, water, and industrial environments, including mining, welding, and battery manufacturing. Manganese (Mn) is an essential metal needed as a cofactor for many enzymes to maintain proper biological functions. Excessive exposure to Mn in high doses can result in a condition known as manganism, which results in disorders of the neurological, cardiac, and pulmonary systems. The aim of this study was to assess cardiac susceptibility to manganese intoxication in Colossoma macropomum subjected to a fixed concentration of 4 mg/mL for a period of up to 96 h. This study used 45 Tambaquis (30.38 ± 3.5 g) divided into five groups of 9 animals/treatment. The treated groups were exposed to the manganese concentration for a period of 24, 48, 72, and 96 h, after which the animals' ECGs were recorded, showing heart rate, R-R interval, P-Q interval, QRS complex duration and S-T interval. The results showed that cardiac activity decreased as the contact time increased, with an increase in the P-Q and S-T intervals. This indicates that the breakdown of circulatory homeostasis in these animals was caused by contact time with manganese.

Keywords: Colossoma macropomum; ECG; manganese; morphographic changes.

Figure 1

Electrocardiographic (ECG) recordings of the control group in Tambaqui, Colossoma macropomum (A). Amplification of the control group ECG with a duration of 5 s (5–10 s) showing the identification of wave elements (P wave, QRS complex, and T wave) and the analyzed parameters, as follows: heart rate, P-Q interval, R-R interval, QRS duration, and S-T interval (B).

Figure 2

Electrocardiographic (ECG) recordings of Colossoma macropomum lasting 300 s and their amplifications (90–100 s) during contact with 4 mg/L of manganese acetate for the following groups: control (A); group treated for 24 h (B); group treated for 48 h (C); group treated for 72 h (D); group treated for 96 h (E); average heart rate (bpm) during each treatment during the 90–100 s interval (F); and average R-R interval (ms) for the treatments, during the 90–100 s interval (G). [ANOVA followed by Tukey’s test (* p < 0.05 ** p < 0.01 and *** p < 0.001 n = 9)].

Figure 3

Recordings showing cardiac activity over 10 s (90–100 s) for the groups treated with manganese at different exposure times: mean P-Q interval (ms) (A); mean QRS complex duration (ms) (B); mean S-T interval (ms) (C). [ANOVA followed by Tukey’s test (* p < 0.05 ** p < 0.01 and *** p < 0.001 n = 9)].

Figure 4

Recordings showing cardiac activity in the interval (190–200 s) of groups with different exposure times to manganese: control group (A); group treated for 24 h (B); group treated for 48 h (C); group treated for 72 h (D); group treated for 96 h (E); heart rate averages (bpm) (F); R-R interval averages (ms) (G); P-Q interval averages (ms) (H); QRS complex duration average (ms) (I); and S-T interval averages (ms) (J). [ANOVA followed by Tukey’s test (* p < 0.05 ** p < 0.01 and *** p < 0.001 n = 9)].

Figure 5

Recordings showing cardiac activity in the interval (290–300 s) during different times of exposure to manganese, as follows: control group (A), group treated for 24 h (B); group treated for 48 h (C); group treated for 72 h (D); group treated for 96 h (E); heart rate averages (bpm) (F); R-R interval averages (ms) (G); P-Q interval averages (ms) (H); QRS complex duration average (ms) (I); and S-T interval averages (ms) (J). [ANOVA followed by Tukey’s test (* p < 0.05 ** p < 0.01 and *** p < 0.001 n = 9)].