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Table 1 Cytostasis and cytotoxicity in BEAS-2B cells exposed to Co3O4P and CoCl2

From: Poorly soluble cobalt oxide particles trigger genotoxicity via multiple pathways

μg mL-1

CBPI

% cytostasis

Apoptotic index

C neg

1.61 ± 0.05

0.00 ± 0.00

0.25 ± 0.06

C pos

1.34 ± 0.08*

44.01 ± 4.04***

0.99 ± 0.06***

LB-3

1.64 ± 0.01

0.00 ± 2.43

0.17 ± 0.07

Co3O4P

1.25

1.62 ± 0.02

0.00 ± 2.57

0.21 ± 0.06

2.50

1.63 ± 0.02

0.00 ± 2.57

0.34 ± 0.16

5

1.59 ± 0.06

2.84 ± 3.67

1.61 ± 0.06***

10

1.48 ± 0.11

20.96 ± 5.57

0.57 ± 0.11

20

1.48 ± 0.12

20.96 ± 6.02

0.60 ± 0.13

100

1.39 ± 0.10

36.68 ± 6.49**

0.62 ± 0.02*

CoCl2

1.25

1.62 ± 0.01

0.00 ± 2.43

0.06 ± 0.06

2.50

1.55 ± 0.03

9.43 ± 2.58

0.39 ± 0.15

5

1.49 ± 0.01

19.34 ± 1.97**

1.02 ± 0.06***

10

1.34 ± 0.05*

44.01 ± 2.73***

0.60 ± 0.07*

 

20

1.20 ± 0.00**

67.07 ± 0.78***

0.10 ± 0.06

  1. The cytostatic effects induced in BEAS-2B after 24 h exposure to Co3O4P and CoCl2 were evaluated by the cytokinesis-block proliferation index (CBPI). Compared with the C neg, only CoCl2 at 10–20 μg mL-1 cobalt induced a slightly significant reduction of CBPI. By contrast, Co3O4P and their control, LB-3, did not exert any cytostatic effect on BEAS-2B cells. The % cytostasis confirmed the toxicity of CoCl2, but highlighted the significance of the exposure to the highest Co3O4P concentration tested (100 μg mL-1 cobalt). Differently, the cytotoxicity evaluated by scoring the apoptotic index showed that Co3O4P and CoCl2 exerted significant effects at 5 μg mL-1, whereas a mild apoptosis was observed after treatment with Co3O4P and CoCl2 (10 μg mL-1 cobalt). The positive control, MMC (0.1 μg mL-1), was cytostatic and cytotoxic. Data are expressed as mean value ± SEM of two independent experiments, each in duplicate. Statistically significant differences from the C neg were determined by one-way ANOVA followed by Holm-Sidak method for comparisons between groups: *p < 0.05, **p < 0.01 and ***p < 0.001